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L161—O-1096 











PULMONARY 


TUBERCULOSIS 


BY 


MAURICE FISHBERG, M.D. 


CLINICAL PROFESSOR OF MEDICINE, UNIVERSITY AND BELLEVUE HOSPITAL MEDICAL 
COLLEGE; CHIEF OF THE TUBERCULOSIS SERVICE, MONTEFIORE HOSPITAL FOR 
CHRONIC DISEASES, AND OF BEDFORD HILL SANATORIUM FOR 
INCIPIENT TUBERCULOSIS 


THIRD EDITION, REVISED AND ENLARGED 


ILLUSTRATED WITH 129 ENGRAVINGS AND 28 PLATES 





LEA & FEBIGER 
PHILADELPHIA AND NEW YORK 






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PREFACE TO THE THIRD EDITION. 


THE cordial reception accorded this book, of which two editions 
have been exhausted within five years, has offered an opportunity for 
radical changes in this new edition with a view of making it a more 
useful guide for the general practitioner as well as the specialist. ‘Two 
new chapters have been introduced: One on the Reciprocal Relations 
Between Pulmonary Tuberculosis and Certain Physiological and 
Pathological Processes, and another on the Medical-legal and Insurance 
Aspects of Tuberculosis. In the former, a detailed discussion of the 
following topics is offered: The reciprocal influences exercised by 
tuberculosis and such physiological processes as growth, puberty, 
sexual functions, fecundation, pregnancy, labor, the puerperium, 
etc. Also a consideration of the coexistence of pulmonary tuber- 
culosis with such pathological processes as extra-thoracic tuberculous 
lesions, diseases of the upper respiratory tract, especially tonsillitis, 
coryza, and the lymphatic diathesis; diseases of the bronchi and 
lung, notably asthma, bronchitis, bronchiectasis, emphysema, pneu- 
monia, etc.; constitutional and metabolic diseases, such as the various 
forms of rheumatism, gout, diabetes, cholelithiasis, nephrolithiasis, 
obesity, and dysfunctions of the endocrine glands, the thyroid, the 
adrenals and the gonads; infectious diseases, notably the exanthemata, 
influenza, typhoid fever, syphilis, etc.; diseases of the gastroin- 
testinal tract, appendicitis, fistula-in-ano, cirrhosis of the liver, etc.; 
and finally, cancer and insanity. It has been borne in mind that 
phthisical patients often live for many years, and that during their 
period of illness they are liable to suffer from various other diseases; 
and therefore the reciprocal relations discussed in this chapter have 
more than theoretical bearing on the symptomatology, course and 
prognosis. As far as the writer knows, this is the first attempt to 
treat this subject in any book or monograph on tuberculosis. 

The new chapter on the Medico-legal and Insurance Aspects of 
Tuberculosis has been included because of the immense interest recently 
displayed by life and health insurance corporations, fraternal organ- 


vi PREFACE TO THE THIRD EDITION 


izations, labor unions, workmen’s compensation commissions, veteran 
rehabilitation boards, ete., in the problems of the diagnosis of tuber- 
culosis and the disability it causes. Traumatic tuberculosis has of 
late very often been considered in courts of law in claims for damages, 
the contention being that injuries were responsible for the origin or 
aggravation of tuberculous lung lesions. 

The fact that the publishers consented to reset the entire book has 
made it possible to make very radical changes in nearly all the chapters. 
Those treating of Phthisiogenesis were rewritten, and emphasis has 
been laid on the problems of the constitutional vs. environmental 
factors in the etiology of tuberculous diseases, because most authorities 
are now in agreement that infection with tubercle bacilli does not 
alone explain fully the origin of phthisis in any of its forms. The 
chapter on artificial pneumothorax has been rewritten and amplified 
in the light of more extended experience, special emphasis being laid 
on the limitations of this mode of treatment. Many new sections 
have been included, the most important being on acute miliary tuber- 
culosis, scrofula, myoidema, the autourine test, phototherapy, artificial 
immunization, etc. Many new illustrations, including roentgeno- 
grams, have been included. 

The author desires to acknowledge indebtedness to his son, Dr. 
Arthur M. Fishberg, for collecting materials, and revising the proof 
of this edition. 


Mor 


FROM THE PREFACE TO THE SECOND 
EDITION. 


Ir is the purpose of this book to supply the general practitioner 
with information concerning the etiology, diagnosis, prognosis and 
treatment of pulmonary tuberculosis, its clinical forms and common 
complications. An experience of over twenty years with the tuber- 
culosis problems in New York City has convinced the author that: 
(1) The physician can, and should, do more than recognize phthisis 
in its earliest or pretuberculous stage and at once consign the patient 
toa sanatorium. (2) That “incipient” does not always mean curable 
tuberculosis, and conversely, that “advanced” disease does not 
necessarily indicate a hopeless outlook. (3) That institutional treat- 
ment is not the only effective method of handling the phthisical 
patient. (4) If all tuberculous persons in this country would con- 
sent to hospitalization, the available institutions would hardly ac- 
commodate ten per cent of eligible patients. (5) Even those treated 
in sanatoriums must be cared for by their family physicians before 
admission and after discharge. (6) Careful home treatment is pro- 
ductive of practically the same immediate and ultimate results as 
institutional treatment, and is less costly to the patient and to the 
community. 

Recent investigations of tuberculous infection have radically changed 
our views on the transmissibility of tuberculosis. On the one hand, 
it was found that patients who indiscriminately expectorate tubercle 
bacilli are a greater menace than has hitherto been suspected. In- 
fants may be infected by mere contact with phthisical persons. On 
the other hand, there is hardly a person living in a large city who has 
escaped infection with tubercle bacilli. In other words, despite the 
vigorous and costly efforts which have been made during the past 
thirty years, the majority of the population in civilized countries 
harbor tubercle bacilli in their bodies. But, what is of more im- 
portance, not every one infected with tubercle bacilli is destined to 
become sick. For this reason, a sharp distinction is made in the 


Vill FROM THE PREFACE TO THE SECOND EDITION 


following chapters between infection and disease, or tuberculosis and 
phthisis. 

Recent research has also shown that infection with tubercle bacilli 
endows an organism with a certain degree of resistance, or even im- 
munity, against further and renewed exogenic infection with the same 
virus. Experimental investigations have proved that it is impossible 
to reinfect a tuberculous animal with tubercle bacilli. Many clinical 
phenomena, which have hitherto baffled those who studied the disease, 
such as the rarity of conjugal phthisis, or of tuberculous disease in those 
living and working among phthisical patients, and of soldiers in the 
armies, are now explained by this immunity of the tuberculous against 
reinfection with tubercle bacilli. Phthisis is at present considered a 
manifestation of immunity. Prophylaxis of infection has been shifted 
to the child, while that of phthisis involves more than prevention of 
infection. 

In the discussion of the clinical aspects of phthisis an attempt has 
been made to elaborate on the constitutional symptoms, which are 
still the sheet-anchor of the physician who is charged with deciding 
whether a patient is ill and in need of treatment. Bacteriology and 
serology are excellent helps in showing whether the patient has been 
infected with tubercle bacilli; skiagraphy reveals airless areas of lung 
tissue; but they do not give conclusive proof that the patient is sick 
and in need of prolonged and costly treatment. We also know that 
unity of causation is not always an indication of unity of resulting 
clinical phenomena in tuberculosis: The clinical picture of tuber- 
culosis in infants is different from that in children; in adults some, 
irrespective of the treatment applied, show a marked tendency to 
sclerosis or fibrosis of the lesion; in others caseation and destruction 
of lung tissue go on progressively; in still others, there is a sluggish 
course, marked by periods of illness alternating with periods of com- 
parative comfort. For these reasons several types of the disease, or 
syndromes, have been described, each of which has not only a dif- 
ferent clinical course but also a different outlook as to recovery, and 
the treatment differs markedly in each form of the disease. 

It appears that the tuberculosis problem has been handled in the 
various armies engaged in the recent World War along the lines men- 
tioned above and some have anticipated that the disease will prove as 
great a menace as many other war plagues, such as typhoid, in- 
fluenza, dysentery, etc. However, despite the fact that only clinical 
tuberculosis has been considered cause for rejection by draft boards, 


FROM THE PREFACE TO THE SECOND EDITION ix 


and tuberculin (the test for infection) has not been applied for diag- 
nostic purposes at all, the number of cases of active tuberculosis in 
the armies has not been excessive, considering that soldiers are of the 
age period when the disease is most likely to occur. This clearly has 
been an experiment on a large scale showing that tuberculous infection 
is not acquired by adults; that infection, which is in the vast majority 
of cases acquired during childhood, is not invariably followed by dis- 
ease, and that only constitutional symptoms decide whether a patient 
is sick with phthisis and in need of treatment. Our rather uncon- 
ventional views on the diagnosis and prophylaxis of phthisis as a disease, 
which have been emphasized in the first edition of this book, have 
thus been fully confirmed. Though infection as a factor in phthisio- 
genesis has been practically disregarded in the various armies engaged 
in the recent war, no visible harm has resulted. 

The treatment recommended in this book is based on experience 
with patients in New York City. Some were living in the congested 
neighborhoods of the Metropolis; others in the better parts of. the’ 
city; still others have been under the author’s care in the hospital. 
A large proportion had been in sanatoriums, but even they had to be 
cared for in their homes before admission and after discharge. Em- 
phasis is laid on the fact that in most cases we can give the patient 
the benefit of modern and approved treatment in his home as well 
as in institutions. The immense utility of sanatorium treatment is 
emphasized and its limitations are enumerated. It is also shown 
that institutional treatment is not the only, nor the best, available 
method of caring for the majority of patients. Experience has taught 
that we can properly house and feed a patient in the city at a much 
less expense than in a sanatorium. 

Medicinal treatment has been alloted some space for the reason that 
it is, in many cases, believed to possess more value than it has been 
accredited by therapeutic nihilists. The most recent method of 
treatment, artificial pneumothorax, has been given at some detail 
because of its efficacy in selected patients in whom everything else 


has failed to afford relief. 
M.F. 





CONTENTS. 


CHAPTER I. 


Tue TUBERCLE BacILui 


CHAPTER II. 


TUBERCULOUS INFECTION . 


CHAPTER III. 


Tue EPIDEMIOLOGY OF TUBERCULOSIS 


CHAPTER IV. 


PHTHISIOGENESIS I. PREDISPOSITION, ENDOGENOUS AND EXOGENOUS 


CHAPTER V. 


PuHTHISIOGENESIS I]. THe PHENOMENA OF IMMUNITY 


CHAPTER VI. 


PaTHOLOGY AND Morspip ANATOMY 


CHAPTER VII. 


SYMPTOMATOLOGY OF PHTHISIS—HISTORY OF THE PATIENT 


CHAPTER VIII. 


CouGH AND EXXPECTORATION 


CHAE ARE Ral 
FEVER AND NIGHTSWEATS . 


CHAPTER X. 


HeMoPTyYSIS . 


CHAPTER XI. 


Symptoms Causep By DISTURBANCES IN THE GASTRO-INTESTINAL 


Tract—THE SkIN—THE JOINTS 


17-39 


40-60 


61-100 


101-137 


138-159 


160-186 


187-194 


195-212 


213-233 


234-256 


x CONTENTS 


CHAPTER XII. 


SympTromMs REFERABLE TO THE CARDIOVASCULAR AND RENAL SYSTEMS . 


CHAPTER XIII. 


NERVOUS SYMPTOMS OF PHTHISIS 


CHAPTER XIV. 
INSPECTION AND PALPATION 


CHAPTER XV. 


PERCUSSION OF THE CHEST IN PHTHISIS . 


CHAPTER XVI. 


AUSCULTATION OF THE CHEST IN PHTHISIS . 


CHAPTER XVII. 


ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


CHAPTER XVIII. 


THe CiinicaL Forms or PHTHIsis 


CHAPTER XIX. 


Curonic Puruisis. INCIPIENT STAGE 


CHAPTER XX. 


CuRoNIc PHTHisis. ADVANCED STAGE , 


CHARTER exo. 
ABORTIVE TUBERCULOSIS . 


CHAPTER XXII. 
Frproi PHTHIsis 


CHAPTER XXIII. 


AcutEe Forms or TUBERCULOSIS . 


CHAPTER XXIV. 


PULMONARY TUBERCULOSIS IN CHILDREN 


CHAPTER XXV. 


PHTHISIS IN THE AGED 


277-288 


289-298 


299-313 


314-335 


336-353 


3594-366 


367-373 


374-395 


396-413 


414-418 


419-428 


429-446 


474-477 


CONTENTS 


CHAPTER XXVI. 


TUBERCULOSIS OF THE PLEURA 


CEVA IR Xe evel Ls 
PNEUMOTHORAX 


CHAPTER XXVIII. 


DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


CHAPTER XXIX. 


CoMPLICATIONS OF PHTHISIS 


CHAPTER XXX. 


RecrprocaL RELATIONS BETWEEN PULMONARY TUBERCULOSIS AND 
CERTAIN PHYSIOLOGICAL AND PATHOLOGICAL PROCESSES 


CHAPTER XXXII. 


PROGNOsIS IN PULMONARY TUBERCULOSIS 


CHAPTER XXXII. 


THe Mepico-LeEGAL AND INSURANCE ASPECTS OF TUBERCULOSIS 


CHAPTER XXXIII. 


Tue INDICATIONS FOR TREATMENT OF PHTHISIS 


CHA PTHR XSex lv. 
PROPHYLAXIS 


CHAPTER XXXvV. 


GENERAL MANAGEMENT OF THE CASE 


CHAR TH Re exe Vils 
Tue Rest Cure 


CHART xXexO evil Le 
OPpEN-AIR TREATMENT . 


CHARTER XOeOviLLT: 
CLIMATIC TREATMENT , 


xiil 


478-520 


521-533 


534-557 


558-574 


575-617 


618-633 


634-651 


652-659 


660-676 


677-686 


686-695 


696-709 


710-722 


XIV CONTENTS 


CHAPTER XXXIX. 


INSTITUTIONAL TREATMENT . . . . . « « «© 2 ge e102 


CHAPTER XL. 
Direretic TREATMENT . . .. 3 3% $ «. « » «© «© « ¢ SeeIeMMMEE(sy eed te 


GCHAPTEReXLL 
MeEpiIcCINAL [CRBATMENT 5 2 6 2 te eee em TE Graria 


CHAPTER XLII. 
SPECIFIC TREATMENT « 3 . «8 6 ee) eg Cee TenU 


CHAPTER XLIII. 


SyMPTOMATIC TREATMENT > 2 am & ORR. 29 5 ee ees 


CHAPTER XLIV. 


OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX . 2 « « « €94-843 


CHAPTER XLV: 
GENERAL TREATMENT OF THE VARIOUS FORMS OF PULMONARY TUBER- 
CULOSIN.. = « 9. & «| SC ele Se SS) 2 SS oe 
CHAPTER XLVI. 


TREATMENT OF COMPLICATIONS, & 99 502). 72 2, ce DU Ot 
INDEX oF AUTHORS ee eer rere se ee aye 


INDEX OF SUBJECTS 6 ee ee eee os errs 





PULMONARY TUBERCULOSIS. 


GHA TERI: 
THE TUBERCLE BACILLI. 


Many ancient and medieval physicians considered pulmonary tuber- 
culosis a contagious disease. In 1865 J. A. Villemin! demonstrated 
experimentally that the disease can be transmitted from one animal 
to another, and from human beings to animals by inoculation of the 
sputum brought up by tuberculous patients. It remained for Robert 
Koch’ to isolate the microérganism which is the infective agent. In 
1882 he published bis first communication describing the morphology, 
staining reactions, cultivation, and the successful animal inoculation 
of pure cultures of the bacilli invariably found in tissues affected with 
tuberculosis. 

The tubercle bacillus is a parasite in the full sense of the word, 
living and thriving only in the bodies of animals and man, and perish- 
ing outside of the animal body. It has not been decided to which 
group of microdrganisms it belongs; in fact, we do not as yet have 
a classification of bacteria which is completely satisfactory to all who 
are competent to judge. It may be said to belong to the group of 
acid-fast bacteria, of which there are many varieties to be mentioned 
farther on, and may be classified with the trichomycetes, while some 
consider it intermediary between the true bacteria and the lower fungi, 
hyphomycetes. 

Morphology.—The morphological variations of the tubercle bacilli 
are dependent on their type and virulence, whether human, bovine, 
or avian, and on the media in which they have been cultivated. In 
film preparations made from cultures, or from sputum expectorated 
by tuberculous patients, the tubercle bacillus appears as a slender 
rod, usually straight, but very often curved, about one-fourth to one- 
half the diameter of a red blood corpuscle, or =} 7 mm. in length, on 


1 Cause et nature de la tuberculose, Gaz. hebd., 2d ser., 1865, p. 50; Bull. de l’Acad. 
de Méd. de Paris, 1865, 31, 211; Etudes sur la tuberculose, preuves rationelles, experi- 
mentelles de sa specificité et de son inoculabilité, Paris, 1868. 

2 Berl. klin. Wehnschr., 1882, 39. An English translation of the complete report, 
originally appearing in Mitt. aus dem Gesundheitsamte, 1887, vol. 2, made by Stanley 
Boyd, has appeared in ‘‘ Recent Essays on Bacteria in Relation to Disease,’’ New Syden- 
ham Society, 1886, pp. 65-201. 

2 


18 THE TUBERCLE BACILLI 


the average. ‘These rods, mostly rounded on the two ends, are seen 
in the preparations from secretions or tissues, singly, in pairs, or in 
heaps, occasionally imbedded in the tissue cells. They are non-motile, 
and have no flagella. Microscopically, an enveloping or capsular, fatty 
or waxy substance can often be made out around each bacillus, espe- 
cially in those which have been artificially cultivated in serum for 
several generations. Some individual bacilli are strikingly pleomor- 
phic, thread, or club-shaped, with thickenings at either or both ends, 
or with filaments passing out from the main rod at right angles, and 
finally in Y-shaped branchings. But these are of no practical signifi- 
cance, because they appear to be simply degenerated types of the 
microorganism, although some look at them as the reverse, the result 
of active growth on a good culture medium, and amid favorable 
biological surroundings. In some individual bacilli, unstained spaces, 
regarded as vacuoles, are seen, giving the rod the appearance of a chain 
of cocci. Bulgingsin various places, showing deeper stain, more resist- 
ant to decolorization, have been considered as spores by some authors. 
But this appears to be erroneous, because they have no stronger 
resistance than the body of the bacillus, and succumb to heat and 
chemicals as fast as the entire rod. The fact that it is speedily killed 
by sunlight also indicates that the tubercle bacillus has no spores. 

Staining.—It has already been noted that the tubercle bacillus is 
surrounded by a fatty or waxy capsule. It is to this sheath that the 
peculiar staining reactions of the bacillus are attributed. 

The tubercle bacillus shows but little affinity for ordinary stains, 
not combining with them unless exposed for a long time, or heated. 
Koch originally stained the bacilli in sections with alkaline methylene 
blue, counterstaining with Bismarck brown. But the first practically 
useful method was that of Ehrlich who found that if the bacilli were 
stained with aniline water and fuchsin, or gentian violet, they subse- 
quently resisted decolorization with nitric acid and alcohol. Hence 
the designation of the bacilli as acid-fast. They were subsequently 
also shown to be alkali fast. The stains in use at present all rest on 
this principle of intense staining followed by decolorization vigorous 
enough to remove the stain from everything on the film but the 





EXPLANATION OF PLATE I.—(Park and Williams.) 
Fig. 1.—Tuberculous lymph node “‘giant cell’’ containing tubercle bacilli ‘human 
type.” Bacilli red, rest of specimen blue. Ziehl-Neelsen stain. X 1000 diam. 

Fia. 2.—Tuberculous sputum from human case. Stainsameas above. > 1000 diam. 

Fig. 3.—Tuberculous sputum, human case. Stained by Hermann’smethod. Tubercle 
bacilli violet, rest of specimen brown. 

Fie. 4.—Pus from tuberculous abscess in cow. ‘Bovine type’ 
same as Figs. 1 and 2. X 1000 diam. 

Fic. 5.—Section through leprous skin showing bacilli in clumps in and out of cells 
and large ‘‘leprous cell’’ containing a ball of bacilli. Stained with Ziehl-Neelsen. 

Fig. 6.—Photograph of human type of tubercle bacilli from sputum. Bacilli in red, 
rest of specimen blue.  X 1000 diam. (Frinkel and Pfeiffer.) 


of bacillus. Stained 


el Oy gg ci 








Note 


or TH 
yniversiTY OF fet 





MUCH’S GRANULES 19 


tubercle bacilli, whose lipoidal sheath tenaciously holds the coloring 
matter. 

The Ziehl- Neelsen method is the most popular. The stain used is 
Ziehl’s carbol-tuchsin solution, prepared as follows: 


Fuchsin ° eer ee OTS OR ee ee ee ee ee 1 gram 
Absolute alcohol eee spl promt: gi an gate @ it ek a ES 25cc¢ 
Carbolic acid, 5 per cent solution er ne eg lt. oe! LOO Ge 


1. Make a rather thin smear on a slide or, preferably, on a cover 
slip. Fix by heat. Flood the staining solution, and steam (not boil) 
over a flame for about three minutes, replacing evaporated solution. 

2. Decolorize with 2 per cent hydrochloric acid, or 10 per cent 
sulphuric acid solution, until the red of the thinner portions has 
altogether disappeared, and the preparation in general appears pink. 

3. Complete the decolorization by washing thoroughly in 95 per 
cent alcohol; then wash in water. 

4. Counterstain with a 1 per cent aqueous solution of methylene 
blue; wash, dry, and examine with an oil-immersion lens. 

Gabbet has modified the Ziehl-Neelsen stain by combining the 
decolorization and counterstaining. ‘He stains as above with Ziehl’s 

carbol-fuchsin, and after allowing, the excess ot stain to drain off, the 
following solution is applied for two or three minutes: 


Methylene blue ... ve eee SS he eee ee eg 2 grams 
Concentrated sulphuric acid bootie! «Sata MN terse ol 10 ce 
Wisave 52 erica s ia. Ld Weeee part. 5 SO en rr oo ae ae ae ek ee OO oye, 


Wash in water and dry. 

With both the above methods the tubercle bacilli appear bright red, 
all else in the field being blue (see Plate I). Gabbet’s method, while 
simpler than that of Ziehl and Neelsen, is not so reliable. For diag- 
nostic purposes the Ziehl-Neelsen method remains the most useful. 

The tubercle bacillus is Gram-positive, but this method of staining 
does not find wide practical application. 

Clinically, it is at times necessary to find tubercle bacilli in specimens 
in which they are very scanty, and the above methods fail to reveal 
them though they are present. In such cases concentration and 
sedimentation of the specimen is practised. For these purposes the 
antiformin method has recently found wide application. The details 
of this procedure are discussed later on (see p. 204). 

It must be mentioned that the tubercle bacilli are not the only 
known acid-fast bacilli. This is one ot the sources of error which, at 
times, interferes with the proper appreciation of acid-fast microérgan- 
isms discovered under the microscope. 

Much’s Granules.— For a long time it has been noted that in the 
lesions in tuberculous cattle, be they as characteristic macroscopically 
as possible, no tubercle bacilli can be found microscopically, but inocu- 
lation experiments prove positive almost invariably, thus showing 


20 THE TUBERCLE BACILLI 


that virulent germs must have been there. Likewise, in human 
pathology, it has often been observed that in cold abscesses no tubercle 
bacilli ean be tound, and again inoculation of the purulent material 
infects animals. These and other facts have led H. Much to suspect 
that there are bacilli which produce specific tuberculous lesions though 
the germs are not acid-fast. Research has, in fact, convinced him 
that he found tubercle bacilli which, while remaining virulent, have 
lost their acid-fast characters. Hans Much,! by whose name these 
microorganisms are generally known, describes two forms of these 
granules: (1) A rod-shaped granular organism; (2) isolated granules; 
both of which cannot be stained by the Ziehl method, but only by the 
Gram method. They are pathogenic to animals and man, and are 
usually found in some cases of slowly progressing chronic phthisis, 
fibroid phthisis, cold abscess, ete. It is thus evident that before con- 
cluding that a given case lacks acid-fast bacilli, and is therefore not 
tuberculous, the Much granules are to be looked for by staining with 
the Gram-Much method. According to William H. Park, true tubercle 
bacilli are probably always present together with the granules in cases 
in which the latter forms are found. 

In this country Charles N. Meader? has made a careful study of 
these granules. In his opinion “the biological relationship of Much’s 
forms of tubercle bacilli is a matter of considerable interest. They 
may be considered as a natural stage in the evolution of the bacillus, 
as the result of degenerative changes, or may be classed as spores 
(7. e., as resisting forms). The accumulated evidence tends to show 
that they are found predominant in tissues of a distinctly fibroid 
character, in old cavities, in pus of cold abscesses, in old cultures, in 
the notably indolent lupus lesions and in sclerosed lymph glands— 
facts which, taken together, mark them as forms assumed under 
unfavorable conditions, whether they be the result of sporulation or 
of degeneration. ‘The same conclusion is suggested by observations 
that, under favorable cultural conditions, they are rapidly replaced 
by Ziehl-staining forms. Against their classification as spores, in the 
commonly accepted sense, is the fact that the granular forms are rather 
less resistant to the action of antiformin than are the Ziehl forms; their 
resistance to other chemical agents has not yet been reported upon. 
It is of interest to note here that the granular forms appear more 
frequently in the bovine than in the human type of bacillus.” 

Cultivation.—The tubercle bacilli are obligatory aérobes; they re- 
quire free oxygen for maintenance of life, activity and propagation. 
In artificial media they grow very slowly, much more slowly than most 
bacteria which are not acid-alcohol-fast; they proliferate very slowly, 
and other saprophytic microérganisms which happen to live with them 
soon outnumber them. Working for the British Royal Commission, 
A. S. Griffith succeeded in perfecting a method which avoids contami- 


1 In Brauer, Sehréder, and Blumenfeld’s Handbuch d. Tuberkulose, 1, 193. 
2 Am. Jour. Med. Sci., 1915, 101, 858. 


POWERS OF RESISTANCE 21 


nation, by the use of antiformin. He inoculates successive cultures of 
tuberculous material, mainly sputum, and antiformin which inhibits, 
or even prevents, the growth of extraneous microorganisms. In this 
country Petroff’s medium is used to facilitate the isolation of tubercle 
bacilli from sputum, feces, and other contaminated sources. This 
selective medium is based on the fact that the lipoid capsule of the 
tubercle bacillus enables it to resist the action of alkalies much better 
than bacteria which lack this means of defense. He also takes advan- 
tage of the selective inhibitory action of certain dyes on the growth of 
bacteria. 

Once the difficulties have been overcome and the bacilli have been 
cultivated, it is rather easy to transplant them to another culture of 
the same medium, and growth is even more luxuriant in the subse- 
quent cultures. Theobald Smith’s method of cultivation on dog serum 
and Dorset’s egg medium, and especially Petroft’s medium, are about 
the best and most used in this country. Pure cultures are best obtained 
from tubercles of animals inoculated with the bacilli. But it is often 
possible to obtain pure cultures from closed tuberculous cavities, from 
lesions of lupus, and even from sputum. 

When cultivated on coagulated dog serum, or bovine serum, or in 
Dorset’s egg medium, especially when to the latter there is added 
glycerin, growth appears usually at the end of ten days at 37° C., 
and within four weeks the characteristic growth may be expected. 
On the glycerin-egg medium the human form of organism produces 
an abundant, wrinkled layer, usually having a yellowish, buff, or 
pinkish color. The growths are seen as more or less elevated colonies 
which may coalesce. On glycerin-agar the growth is more rapid than 
on serum, and appears as a thick, white layer, becoming yellowish. 
Tubercle bacilli also flourish in glycerin-potato medium. 

Powers of Resistance.—The tubercle bacilli grow best at the tem- 
perature of the human body, 37° to 38° C., but growth is not abolished 
at 29° to 42° C. From a practical standpoint it is important to men- 
tion that they are not killed when exposed to moist heat of 50° C. 
for less than twelve hours, but heating to 55° C. for four to six hours 
does destroy them. They are also killed when exposed to moist heat 
of 60° C. tor one-half hour, and in fifteen minutes at 70° C.; in five 
minutes at 80° to 90° C., and in one minute at 95° C. With sputum, 
conditions are different: the mucus protects the bacilli and it requires 
more time to destroy them with heat. However, five minutes’ boiling 
is sufficient to kill the bacilli under all circumstances. 

Another practical point is that in milk, tubercle bacilli resist the 
action of heat with greater tenacity than in pure liquid cultures, or 
even in sputum. From many careful experiments it appears that heat- 
ing milk for thirty to forty minutes, at a temperature of 65° to 70° C., 
or boiling for three minutes, destroys tubercle bacilli. Especially 
resistant are the bacilli when the milk is heated in an open vessel and 
a pellicle forms on the top of the fluid. This protects the bacilli against 


22 THE TUBERCLE BACILLI 


a temperature of 60° C. for an hour. William H. Park explains this 
by the tact that the upper parts of the fluid are not heated to the 
same degree as the lower, and some bacilli may survive. At any rate, 
it is important that pasteurization should be done in closed vessels. 
In butter the virulence of the bacilli is greatly diminished and even 
abolished when in contact for a long time. In fact, they die out within 
a few weeks, as a rule. The reasons for this phenomenon are not 
clear. On the other hand, Schroeder and Cotton have found living 
tubercle bacilli retaining their virulence for one hundred and sixty days 
in salted butter when kept without ice in a house cellar; and Mohler, 
Washburn, and Doane found that they survived a year in cheese. 
In thoroughly boiled or roasted meat the bacilli are destroyed; but 
in the rare portions they may survive. Sausages, etc., made of 
uncooked meat, may contain living tubercle bacilli. 

Dry heat is less potent in destroying tubercle bacilli; circulating 
steam requires one-half hour for this purpose, while bacilli in dried 
sputum can withstand a temperature of 100° C. for an hour. On 
the other hand, cold does not destroy their virulence, and freezing, 
with subsequent thawing, does not harm them very much. 

As has already been mentioned, the fatty substances and wax con- 
tained in the tubercle bacilli protect them to a certain degree from 
the effects of desiccation, and from the bactericidal action of the 
normal body cells, although for growth and proliferation they require 
moisture. When dried and pulverized by being converted into dust, 
as is often the case with tuberculous sputum eliminated indiscrimi- 
nately by careless patients, most of the bacilli succumb, but some have 
been found to resist desiccation at ordinary temperature for months. 

In this connection it must be borne in mind that the action of hght 
is an important factor. It has been ascertained that light, especially 
sunlight, decomposes the fatty substances in the bacilli and thus 
destroys them altogether. When cultures are exposed to direct sun- 
light for a couple of hours, the vitality as well as the virulence of the 
tubercle bacilli is destroyed; in sputum the bacilli are protected by 
the mucus, and it requires a longer time for their destruction. Some 
maintain that their virulence is destroyed with only partial loss of 
vitality. 

On the other hand, recent investigations by Técon' show that 
tubercle bacilli expectorated in sputum remained virulent for as long 
as nine days though exposed to the action of the sun in summer, and 
he concludes that the sterilizing action of sun rays has been over- 
estimated; in the clumps of sputum they may survive for days. 

These facts have been utilized in attempts at prophylaxis of tuber- 
culosis. The danger of expectoration of tuberculous sputum is less 
in streets and in well ventilated rooms where bright light, especially 
sunshine, sooner or later renders it harmless, than in dark rooms 


1 Paris Médicale, 1920, 10, 33. 


POWERS OF RESISTANCE 93 


where the bacilli may retain their vitality and virulence for as long 
as one year, and even drying does not harm them very much. 

On the whole, tubercle bacilli may retain their vitality for a con- 
siderable time if not in exceptionally unfavorable surroundings. In 
the latter case their growth is soon hampered, and they cannot suc- 
cessfully be transferered by inoculation to another culture medium; 
but they may retain their virulence much longer and cause disease 
when inoculated into animals. After several months, however, even 
this wanes, and after six months this property is completely lost. 
Raw! demonstrated that pure cultures of human, bovine, and avian 
bacilli may retain all their characteristics and selective appearances 
for as long as twelve years when regular subculturing on artificial 
media containing glycerin is practised. In laboratories it has been 
found by experience that it is safer to reinoculate cultures every four 
to six weeks. Exceptionally, cultures have been found alive and viru- 
lent after two years. ‘This 1s especially the case with potato and bouil- 
lon cultures which have been kept under favorable conditions, as to 
heat, moisture, ete., while in serum and glycerin cultures the bacilli 
do not survive so long. 

Cornet found that serum cultures remain alive for about six months, 
while glycerin-agar cultures are often partially, or wholly, dead in six 
to eight weeks. There seems also to be some difference in this respect 
between the various types of tubercle bacilli: Maffucci states that 
avian bacilli may remain alive for two years, and Strauss found that 
cultures of human tubercle bacilli are only exceptionally capable of 
reproduction after five to six months; after eight to twelve months 
they fail regularly. Theobald Smith? found that a culture three months 
old failed, as a rule, to yield successful subcultures, and that tubercle 
bacilli, of both human and bovine types, when kept in fully developed 
cultures at 40° to 50° F., may remain infectious to guinea-pigs for from 
seven to nineteen months, but the number of bacilli surviving in such 
cultures is relatively small. Delépine’s® experience has been that 
tubercle bacilli retain some of their pathogenicity as long as 500 days 
if left in the dark in milk at a low temperature, below 6° C.; but 
after being kept thus for four and one-half years these bacilli were no 
longer pathogenic to guinea-pigs. It is, however, important to bear 
in mind, when considering prophylaxis, that when tubercle bacilli in 
sputum are deposited in dark rooms they may retain their vitality and 
power to cause disease for as long as three hundred and nine days, as 
has been found by Soparkar.t The oldest tuberculous sputum which 
has been investigated was that reported by Newell Bly Burns.2 He 
examined sputum twenty-two years old and found that the bacilli re- 


1 Lancet, 1919, 1, 376. 

2 Jour. Med. Research, 1913, 28, 91. 

3 Ann. de l’Inst. Pasteur, Paris, 1916, 30, 600. 
4 Indian Jour. of Med. Research, 1916, 4, 62. 
5 Amer. Review of Tuberc., 1917, 1, 484. 


24 THE TUBERCLE BACILLI 


tained their staining qualities, but lost completely their power to grow 
and their pathogenicity. 

Tubercle bacilli display great powers of resistance to the action of 
the products of other bacterial growths, in spite of the fact that they 
have no spores. They may survive for months in souring milk, in 
sewage and in water, and in putrefying matter generally, especially 
sputum. Lawrason Brown, 5. A. Petroff and F. H. Heise! found viru- 
lent tubercle bacilli in the water of the Saranac River, into which 
the sewerage system of Saranac Lake empties. Every sample of water 
taken from below the surface, from the outlet of the sewer to a point 
three and a half miles down the stream, showed the presence of acid- 
fast organisms. No acid-fast organisms were found above the outlet 
or twelve miles below the outlet. The bacilli were believed to be 
derived from the feces of the numerous tuberculous individuals in 
Saranac. In fact, where no particles of feces were discovered in the 
water, no viable tubercle bacilli were found. 

Virulence.—Long before the discovery of the tubercle bacillus it 
was known that certain diseases in animals were of the same character 
as human tuberculosis, and attributed to the same virus. Jlenke, in 
1846, emphasized the danger of milk from tuberculous cattle as an 
infective agent to human beings, and Villemin, in 1865, showed by 
animal experiment that tuberculous disease in man and animals is 
identical in character. With the study of the virulence of the tubercle 
bacillus it was found that it is pathogenic to many species of animals. 
In some, tuberculosis is known to occur spontaneously, while others 
may be infected artificially. There appear to be significant differences 
in the results of such experimental infections, depending or the method 
of inoculation of the virus—injections into the subcutaneous tissues, 
into the peritoneum, into the anterior chamber of the eye, intrave- 
nously, by feeding animals with bacilli, or compelling them to inhale the 
bacilli with inspired air, and also according to the origin of the bacilli. 
However, virulence is hardly, if at all, influenced by passage through: 
animals. Baldwin, Krause, and others worked with a culture for over 
ten years and they never noted any variation of its virulence. 

Tubercle bacilli obtained from different cases of human tuberculosis 
often show differences in their virulence according to the strain. Some 
authors have observed differences in virulence according to the origin 
of the bacilli from various tuberculous diseases, and they have then 
attempted to attribute the numerous clinical phenomena of this 
disease to the degrees in virulence of the virus. But, so far, no conclu- 
sive proof for such assumptions have been brought forward. Inocu- 
lating numerous animals with sputum derived from one tuberculous 
patient, there are often observed different results, showing that the 
susceptibility of the individual animal must be reckoned with. More- 


1 Tr. Nat. Assn. Prevent. Tuberc., 1916, 12, 286. 


HUMAN, BOVINE, AND AVIAN BACILLI 20 


over, we should not apply, without careful consideration, results of 
animal experimentation to clinical phenomena in human beings. 

When the bacilli obtained from different animals are compared, the 
difference in their virulence are even more striking. For this reason 
there have been described different species, varieties or strains of 
tubercle bacilli, although some authors maintain that the differences 
in cultural and virulence characteristics are acquired while the micro- 
organisms are sojourning in the host by adaptation to the conditions 
favorable for their growth. 


HUMAN, BOVINE, AND AVIAN BACILLI. 


In the early history of the scientific investigation of tuberculous 
infection it was already noted that there are some differences between 
human and bovine tubercle. Villemin was the first to mention these 
differences. ‘“‘ We must note that none of our rabbits,” he said, “ inocu- 
lated with human tubercle have presented a tuberculization so rapid 
and generalized as that which we have obtained with material from 
the cow. At first we were inclined to regard this as fortuitous, but 
subsequent experiment led us to suppose that the tubercle of the bovine 
race inoculated into rabbits possesses a much greater activity than that 
obtained from man. It may be supposed that, like all virulent matter, 
the tuberculous matter is the more virulent the more the affinity of 
the animal supplying the virus and the animal receiving it.” This 
apparently was entirely forgotten, until Nocard and Roux, and Rivolta 
and Maffucci again rediscovered it while doing inoculation experiments 
with tubercle bacilli derived from humans and from cattle. 

It remained, however, for Theobald Smith! to make the first care- 
ful study of differences in morphological, cultural, and pathogenic 
types of tubercle bacilli. In 1898 he showed that there are differences 
between the bacilli isolated from human beings, when compared with 
those isolated from cattle. His designation of the former as “human,” 
and the latter as “bovine,” has since been generally accepted. In 
1901 Robert Koch also announced that his studies led him to the con- 
viction that human and bovine tuberculosis are not identical; that the 
bovine bacilli are, in fact, not pathogenic to man, and that no special 
measures need be taken to protect man against the consumption of 
milk and meat from tuberculous cattle. Considering the commercial 
interest which is centered around this problem, in addition to the 
problem of human infection, it is clear why studies along these lines 
have been in abundance during recent years. 

Still other types of bacilli have been found. Rivolta and Maffucci 
have shown that there are certain morphological and biological dif- 
ferences between the tubercle bacilli found in birds and those in 
human beings. Theobald Smith continued the investigation of the 


1 Jour. Exper. Med., 1898, 3, 451. 


26 THE TUBERCLE BACILLI 


problem and arrived at the conclusion that bacilli from human sources 
are not clearly identical in every respect with those obtained from 
bovine sources. Official bodies of the Imperial Department of Health 
in Germany, a Royal Commission in England, and Dr. William H. 
Park, for the New York City Department of Health, have thoroughly 
studied the problem, each from a different angle. The result is that 
we are at present in a position to state conclusively that there is more 
than one variety of tubercle bacillus. 

The conclusions of the British Royal Commission are to the effect 
that “for the purpose of description it is advantageous to distin- 
guish three types of tubercle bacilli, recognizable by their individual 
characters. ‘These are the human, the bovine, and the avian. The 
human type, although so named, is not the only one found in cases 
of tuberculosis in man. It is the organism present in the majority 
of such cases, but in some cases of human disease the bacilli present 
are of the bovine type, and in others the bacilli have special charac- 
ters distinguishing them from each of the three principal types. In 
natural cases of tuberculosis in cattle the only type of bacillus present 
is. the bovine type.” William H. Park! concludes from his extensive 
study of the subject that “tubercle bacilli, as isolated from man, fall 
into two groups. One of these groups is identical in all its characters 
with those found in cattle. That is, all tubercle bacilli from man and 
cattle fall into two groups, which have been designated the human 
and bovine types.” 





Fic. 1.—Tubercle bacilli, homan. XX 1000 diameters. (Park and Williams.) 


Human Bacillii—The human variety grows on all culture media 
quickly and luxuriantly; the addition of glycerin enhances its 
growth. On glycerin bouillon growth is seen during the first few days, 
and within three weeks there is seen a pellicle on the surface of the 
culture which spreads laterally and reaches the glass walls. The pellicle 
is fragile and its surface wrinkled. Morphologically, the human bacilli, 
when grown on serum cultures, appear as long, straight or curved rods 
which are unevenly stained. 


1 Jour. Med. Research, 1911, 20, 313; 1912, 22, 109. 


HUMAN, BOVINE, AND AVIAN BACILLI 27 


In general it may be stated that the virulence of human bacilli is 
rather low in various animals. Guinea-pigs are very susceptible and 
may be infected in various ways, even by rubbing the bacilli into the 
shaved skin of the abdomen. Rabbits are, however, less susceptible. 
Even when a milligram of bacilli is injected into a vein of the ear 
there is only produced a chronic lesion which may heal; subcutaneous 
injection produces an infiltration at the point inoculated, which soon 
softens and empties itself through a fistulous opening, or may even 
be absorbed. The regional lymph glands swell, but do not caseate. 
At times, but not in every case, there may thus be produced a chronic 
infection of the lungs in the rabbit. Intraperitoneal inoculation pro- 
duces tuberculous peritonitis, which may extend along the diaphragm; 
infection of the anterior chamber of the eye produces a lesion which 
develops more slowly than when bovine bacilli are used. Cattle 
are infected when large doses are injected intravenously. But with 
subcutaneous infection there is produced only an infiltration at the 
point inoculated, which soon suppurates and heals. The regional 
lymph glands swell up and at times become calcified. Feeding calves 
with human bacilli never produces any progressive disease. Pigs, dogs, 
eats, and sheep are not at all affected by human bacilli, while mon- 
keys are very susceptible. Some species of birds are also susceptible. 





Fic. 2.—Tubercle bacilli, bovine. > 1000 diameters. (Park and Williams.) 


Bovine Bacilli.—The bovine bacilli are very difficult to cultivate; 
it appears that the addition of glycerin to the culture medium slackens 
their growth. On glycerin bouillon growth is very slow. A thin 
pellicle is formed which spreads all over the surface within four to 
eight weeks, but it may remain limited to the center of the surface. 
Only rarely are a few verrucose thickenings formed on the surface. 
After several transplantations they may show greater tendencies to 
grow. Morphologically, they appear as shorter, thicker, are more 
evenly stained than the human variety, and usually bent, showing bead- 
ing and irregularities in staining. Park, who has done excellent work 
along these lines, says: “Although one could in many instances make 
a probable diagnosis of type from an inspection of the smear, the 


28 THE TUBERCLE BACILLI 


number of intermediate gradations in morphological differences rob 
it of nearly all its practical value.” 

The bovine bacilli are more virulent for rabbits, calves, and swine 
than the human. Guinea-pigs are just as susceptible to them as 
they are to the human variety, but in addition they are killed, or 
become acutely and progressively sick, when infected with small 
doses of bovine bacilli. The difference in the virulence of the two 
types is well seen in the rabbit. The bovine type of virus causes in 
every instance generalized miliary tuberculosis, progressive, terminat- 
ing in death of the animal. “Human virus injected in the same 
amount produces either no disease at all, or lesions of varying severity 
in the lungs or kidneys, or both, and never causes generalized miliary 
tuberculosis. Even with 1 mg., that is, one hundred times as much, 
the lesions are usually confined to the same organs, and though there 
is a very slight tendency to generalization with this dose, there is 
never a generalization showing a progressive nature. Rabbits injected 
even with the larger dose live indefinitely, and, if death should occur, 
the tuberculous lesions are usually not extensive enough to say that 
the animal died of the disease.”’ (Park and Krumwiede.) 

Cattle are very susceptible to the bovine virus, and after intra- 
venous injection perish from generalized tuberculosis within three or 
four weeks. Intraperitoneal, intraocular, and intramammary inocu- 
lation also cause generalized and fatal tuberculosis. Feeding cattle 
with even small doses of pure culture of bovine tubercle bacilli 
causes tuberculous disease of the intestines, followed by tuberculous 
lymphangitis and lymphadenitis of the mesentery; the disease spreads 
to other lymph glands, serous membranes, and lungs. Inhalation pro- 
duces caseous pneumonia. After subcutaneous injections there is 
produced an infiltration at the point inoculated, swelling of the regional 
lymph glands, and generalized tuberculosis, the animal perishing 
within two or three months. Pigs, sheep, goats, cats, and monkeys are 
very susceptible; dogs, rats, and mice are more or less refractory. Some 
species of birds are susceptible, but chickens show complete resistance. 

Avian Bacilli.—On glycerin agar and on serum their growth is more 
luxuriant, appears more moist, or slimy, than observed in mammalian 
bacilli, and they produce an orange pigment. They grow at the tem- 
perature of 41° C., which stops the growth of mammalian tubercle 
bacilli. Morphologically, the differences are insignificant. The Royal 
Commission found that rabbits, rats, and mice are the only mammals 
susceptible to inoculation with avian tubercle bacilli. Fowls are very 
susceptible when fed with portions of the organs containing avian 
bacilli, but they may consume enormous quantities of phthisical spu- 
tum without becoming tuberculous. On the other hand, the parrot 
is susceptible to both human and bovine bacilli as well as to avian, 
and spontaneous tuberculosis may be due to any of the types. Tuber- 
culosis is very common among domesticated birds and there have been 
observed veritable epidemics of the disease in poultry yards. 


HUMAN, BOVINE, AND AVIAN BACILLI 29 


Lamallerée, Lowenstein, Kruse, Lydia Rabinowitsch, and Max 
Koch have reported cases of tuberculosis in human beings caused by 
avian tubercle bacilli.t 

Tubercle Bacilli of Cold-blooded Animals.—Certain diseases ob- 
served in worms, lizards, frogs, turtles, snakes, and fish have great 
resemblance to human tuberculosis and in many cases acid-fast bacilli 
have been isolated. These microdrganisms grow luxuriantly at the 
room temperature, the growth being thick and moist like that of 
avian bacilli, and a higher temperature than 30° C. inhibits their 
growth. While they do not grow at the body temperature, it appears 
that some have been able to acclimate them to a temperature of 36° 
C. Weber and Taute have cultivated this microédrganism from mud, 
and also from healthy frogs. ‘They therefore conclude that these 
acid-fast bacilli have nothing in common with tubercle bacilli, but 
they are saprophytes which may be found in healthy animals and in 
the soil. Others, however, consider them as true pathogenic bacilli 
of cold-blooded animals, or such as have become attenuated in their 
virulence by a long residence in, and adaptation to growth at a lower 
temperature. 

Attempts have been made to use these bacilli for the purpose of 
immunization against infection with mammalian tubercle bacilli, but 
they were unsuccessful. F. F. Friedmann has even claimed that 
bacilli obtained from turtles are curative of existing tuberculous 
disease, but the results obtained have not justified in the slightest his 
pretensions. 

Other Acid-fast Bacilli; Pseudotubercle Bacilli.— The tubercle bacilli 
are not the only variety ot microérganisms which, once stained, refuse 
to be decolorized by acids and alcohol. There have been found many 
others presenting the same staining reactions as the tubercle bacilli, 
and there is no doubt that they may bring about confusion in diagnosis. 
Of these we may mention the following: 

The most important clinically is the smegma bacillus, a slender, 
slightly curved rod, not unlike the tubercle bacillus, but distinctly 
shorter. It resists the action of acids and alcohol after staining. It 
is found in the secretions of the external genitals, mamme, etc., espe- 
cially when these secretions contain fatty matter. There have been 
reported cases in which extirpation of kidneys was performed as a result 
of mistaking these microdrganisms for tubercle bacilli. It has also 
been described as occurring in the sputum, and in the pharyngeal and 
tonsillar secretions on rare occasions. It is somewhat more readily 
stained than is the tubercle bacillus, and considerably more easy to 
decolorize. For the differentiation of the smegma from the tubercle 
bacillus, Pappenheim devised a stain depending on the fact that the 
former is decolorized by prolonged exposure to rosolic acid and alcohol, 
while the latter is not. The smegma bacillus is probably identical with 


1 For details see, E. Lowenstein: Vorlesungen tiber Tuberkulose, Jena, 1920, p. 63. 





30 THE TUBERCLE BACILLI 


the acid-fast bacillus discovered by Lustgarten in 1884, and believed 
by him to be the cause of syphilis. 

The Hansen bacillus, which is the cause of leprosy, is also acid-fast. 
Morphologically, it is very similar to the tubercle bacillus, though a 
little plumper and less apt to have a beaded appearance. In staining 
properties it only differs quantitatively from the tubercle bacillus, not 
being so strongly acid-fast. 

Méller’s grass bacilli are found in infusions of timothy-grass (phleum 
pratense), resemble morphologically the tubercle bacilli, and are acid- 
fast. Inoculations produce lesions exquisitely resembling tubercles. 

Moller has also described a bacillus found in milk, at times in pas- 
teurized milk, according to Kuthy. Its similarity to the tubercle 
bacillus is more pronounced than most of the other pseudotubercle 
bacilli. Inoculated into the peritoneal cavity of guinea-pigs, white 
mice, and frogs, these pseudotubercle bacilli obtained from tonsils, 
tongue, and throat, produced lesions which had great similarity, 
microscopically, to real tubercles, but they never spread beyond these 
areas. The only difference which can be discovered is that while 
genuine tubercles are of a proliferative character, these pseudotubercles 
are of a more exudative and inflammatory character, showing a ten- 
dency to abscess formation. 

There have been isolated microérganisms from cow’s milk, butter, 
and from the surface of domestic animals, which morphologically, 
culturally, and even on inoculation, resemble tubercle bacilli. The 
butter bacilli, first described by Petri and Rabinowitsch, may be 
mistaken for tubercle bacilli even when judged by the lesions they 
produce on inoculation into guinea-pigs. 

There have also been isolated acid-fast rods from the excrement of 
cattle, swine, sheep, guinea-pigs, white mice, chickens, dogs, ete. In 
fact, they are so frequent in the soil that any being, or thing, coming 
in contact with the soil is likely to have acid-fast rods, when carefully 
examined with the microscope. ‘They were also found in the dust of 
human dwellings, in tap water, in centrifuge tubes, in the sediment of 
distilled water in laboratory flasks; finally, in cerumal tartar on the 
teeth, and in the cerumen of the human ear, and also in the mouth- 
pieces of musical instruments. 

The acid-fast rods found in the mouth pieces of musical instruments 
have recently been studied by Bruno Lange,! who believes that they 
are derived from the fat used in lubricating the instruments, or the 
water used for washing them, or from the mouths of the musicians. 
These saprophytes appear to be very widely distributed. According 
to Lange they proliferate very slowly, and morphologically they are 
akin to the acid-fast bacilli derived from turtles; they are short and 
plump, as a rule; but long and slender forms, exactly like tubercle 
bacilli, are at times encountered. They grow best at a temperature 


1 Deut. med. Wehnschr., 1920, 46, 763. 


HUMAN, BOVINE, AND AVIAN BACILLI dl 


between 20° and 30° C.; some grow at 0° to 37° C. All culture media 
are suitable, but those containing glycerin are best. 

It is interesting that inoculation of material containing acid-fast 
bacilli derived from musical instruments into guinea-pigs produced no 
general reaction, or constitutional disease, nor could it be established 
that these organisms proliferated within the body. Inoculation of pure 
cultures into guinea-pigs and white mice produced abscesses when the 
dose was large. After intraperitoneal injection, fibrinous and purulent 
peritonitis resulted which, however, healed with scar formation. 
Repeated inoculations caused death of the animal. At times the tissue 
reactions reminded of the gross appearances of real tuberculous lesions. 
It is noteworthy that inoculation of large doses caused swelling, not 
only of the regional lymph glands, but also of other glands, the axillary, 
bronchial and mesenteric. 

It is very difficult to differentiate the pathogenic from the non-pathogenic 
acid-fast rods, or bacilli, microscopically; even the most experienced often 
cannot tell the difference when examining a smear on a slide, which shows 
that clinically, when the non-pathogenic bacilli are found, they are 
apt to lead to erroneous diagnoses. So far bacteriologists have relied 
on results of inoculation experiments: With the pathogenic bacilli 
tuberculous lesions are produced in guinea-pigs, while the others are 
harmless. Recently Schlossberger and Pfannenstiel' have shown that 
differentiation may be attempted by a determination of the optimal 
temperature for their growth, and the temperature limits of their 
growth. Pathogenic tubercle bacilli do not grow at a temperature 
higher than 42° C., while all non-pathogenic acid-fast cultures, with the 
exception of the “trumpet bacilli” (see p. 30), keep on growing at 
50° C. They also found that pathogenic tubercle bacilli from cold- 
blooded animals stop growing at 37° C., thus indicating that the turtle 
bacilli, which Friedmann has been using for therapeutic purposes, 
cannot be regarded as genuine tubercle bacilli from cold-blooded 
animals. 

It seems that the cellular structure of these pseudotubercle bacilli 
is closely related to that of the pathogenic microérganisms, at any 
rate, chemically, as is clearly shown by their similarity in staining 
reactions, and their effects locally when inoculated into animals. 
Some produce lesions not unlike those produced by the virulent tubercle 
bacilli, excepting that the general toxemia is lacking, and the lesion 
does not extend beyond the point of inoculation, though to this there 
are exceptions, as is the case with the trumpet bacilli. It has been 
stated that animals sensitized to any type of the non-virulent acid-fast 
bacilli are also to some degree sensitized to the virulent form. But 
whether they are phylogenetically related, 7. e., whether they have 
evolved from a common ancestry, has not been established. That 
they have not differentiated because of the variety of environment in 


1 Deut. med. Wehnschr., 1920, 46, 1213. 


32 THE TUBERCLE BACILLI 


which they have lived for many generations, appears to be proved by 
the fact that efforts at making them pathogenic by passage through 
the bodies of various animals for several generations have failed. 
However, Igersheimer and Schlossberger,! recently succeeded in ren- 
dering them pathogenic by successive passage, and prolonged sojourn 
in guinea-pigs; the lesions produced were like those of genuine tubercle 
bacilli. Lange,? working with various other acid-fast saprophytes, such 
as turtle bacilli, trumpet bacilli, ete., could not obtain these results. 


OCCURRENCE OF THE VARIOUS TYPES OF TUBERCLE 
BACILLI. 


The human type of tubercle bacilli is found in the vast majority 
of cases of all forms of tuberculosis in human beings; in adults, pul- 
monary phthisis is almost exclusively caused by this virus. In spon- 
taneous tuberculosis in hogs a small percentage shows this type of 
bacilli, and many species of animals, especially those coming in contact 
with man, also are occasionally infected with human tubercle bacilli. 
This is the case with parrots and some animals in zoélogical gardens 
in cities, like lions, antelopes, gnu, chimpanzees, macacus rhesus, etc., 
have been found infected with the human bacilli. The dog, rat, and 
mouse are practically immune, while the calf, rabbit, hog, and goat 
occupy intermediate positions. 

The bovine type of tubercle bacilli is responsible for disease in 
domestic animals, as cattle, sheep, goats, horses, etc. In most cases 
of tuberculosis in pigs, cats, and dogs, and in many cases in monkeys, 
the bovine bacilli are found. 

The avian type is found in the vast majority of tuberculous infec- 
tions in birds. Not only are fowls affected, but also birds in zodlogical 
gardens are susceptible and are often sick as the result of infection 
with this virus. Spontaneous tuberculosis in horses, swine, monkeys, 
cattle, mice, and rats has been found, at times, to be due to this type 
of bacillus. We have already mentioned that they, in extremely rare 
instances, have caused disease in human beings. 

Bovine Type of Bacillus Tuberculosis in Man.—Of great impor- 
tance is the occurrence of bovine infection in human beings. Since 
Koch stated the bovine bacilli were not at all identical with 
the human, and that they were not pathogenic to man, various in- 
vestigations have been made with the result that Koch was, on the 
whole, not sustained. There is evidence to the effect that many 
cases of tuberculosis in human beings, especially in children, are due 
to the bovine virus. The largest collection of cases of tuberculosis of 
various forms was published by B. Méller,? comprising 2048 patients. 
In adults only 2.1 per cent of bovine bacilli were found, and most 


1 Deut. med. Wehnschr., 1921, 47, 526. 
2 [bid., p. 528. 
3 Veroff. Koch-Stiftung, 1916, Hefte 11 and 12, 


THE VARIOUS TYPES OF TUBERCLE BACILLI 30 


of these were cases of abdominal and glandular disease, “ digestive 
tuberculosis.” In tuberculosis ot the lungs only 0.51 per cent showed 
bovine bacilli. Of 186 cases of bovine infection, 145 were found in 
children under sixteen years of age, and of these, 101 had disease of 
the abdominal viscera, especially the cervical and abdominal glands. 
He also found that when bovine infection occurs in humans, it pursues 
a favorable and benign course. Another collection of reported cases 
was published by Park and Krumwiede, embracing 940 instances of 
tuberculosis carefully studied as to the type of organism present, and it 
appears that in adults, sixteen years of age and over, only tuberculosis 
of the skin, abdominal organs, and general tuberculosis of alimentary 
origin may, at times, be caused by bovine bacilli. It is, however, a 
fact that but comparatively few cases have been investigated, and 
there is a lurking suspicion that in a larger series of cases the propor- 
tion would be much smaller. On the other hand, among 778 cases 
of pulmonary tuberculosis only 3, or 0.4 per cent were found with 
bovine bacilli, showing conclusively that as regards phthisis, the bovine 
type of bacilli is not to be considered a vital factor in the patho- 
genesis of the disease. 


PERCENTAGE OF INCIDENCE OF BOvINE TUBERCULOSIS IN 940 CAsEs, OF WHICH 7/8 
WERE PULMONARY TUBERCULOSIS (PARK AND KRUMWIEDE). 


Adults 16 years Children 5 Children un- 


and over. to 16 years. der 5 years. 
Diagnosis. Per cent. Per cent. Per cent, 
Pulmonary tuberculosis 0.4 0.0 2.8 
Tuberculous adenitis, cervical . Det 38.0 61.0 
Abdominal tuberculosis 20.0 Dono) 58.0 
Generalized tuberculosis, alimentary 0 avin 14.0 5720 47.0 
Generalized tuberculosis : 0.0 16.0 8.6 
Generalized tuberculosis, including meninges, Tate 
mentary origin 0.0 0.0 66.0 
Tuberculous meningitis aa or without penerals 
ized lesions other than preceding) 0.0 0.0 4.6 
Tuberculosis of bones and joints Bhiee 3.0 6.8 0.0 
Tuberculosis of skin ee ee eee 8 () 60.0 0.0 


In children the picture is different. Under five years of age 61 per 
cent of cervical tuberculous adenitis, 58 per cent of abdominal tuber- 
culosis, and 66 per cent of the generalized tuberculosis and meningitis, 
and of alimentary origin, are caused by the bovine virus. 

More recent investigators have confirmed the predisposition to 
bovine infection during childhood, and the strong immunity displayed 
by adults, who are almost exclusively infected by the human types of 
bacilli. Thus, A. Stanley Griffith,! in his latest report on the occurrence 
of bovine bacilli in human beings, found that among 1068 persons 
examined, 803 showed human bacillus infections; 194 bovine bacillus 
infections, and 5 a mixed infection. According to age, the following 
table gives details: 


1 Jour. of Path. and Bacteriol., 1920, 23, 129. 


o4 THE TUBERCLE BACILLI 





Number of Per cent of 
Age period. cases. bovine bacilli. 
Oto. . 5 years:.1 * 37.0% Dee Oe Po Ree 37.55 
5.10.10 ve tice sok Beene ye ee SSS 29.45 
TO:too 160 ee 20: ger oe el) 14.66 
16upward “ ae at eos: 6.25 
Total.) pgp 3B ee hee ee ee re eS 20.70 


Of the various forms of tuberculous disease in which bovine tubercle 
bacilli were found by Griffith the following are of interest: Bones and 
joints, 19.7 per cent; genito-urinary organs, 17.65 per cent; cervical 
glands, 46.3 per cent; meninges, 20 per cent; scrofulodermia, 34.65 
per cent; lupus, 48.9 per cent. 

Investigations for the Local Government Board showed that 18.4 
per cent of the children under ten years who died of tuberculosis, or 
other causes, were infected with bovine tubercle bacilli. The predi- 
lection of the glands by the bovine bacilli is also shown in the following 
figures: In a series of cervical gland cases investigated by Griffith,' 
71.4 per cent (20 out of 26) of the children under ten, 38.5 per cent 
of those between ten and fifteen years, and 29.6 per cent of persons 
over fifteen were found to have been infected with bovine tubercle 
bacilli. Mitchell? states that 90 per cent of the cases of cervical gland 
tuberculosis in Edinburgh children under twelve investigated by him 
were due to bovine bacilli. 

Cobbett,? after careful study of available evidence, arrives at the 
conclusion that “we do not yet possess the evidence which will 
enable a final verdict to be pronounced” as to the significance of 
bovine infection in human tuberculosis. One thing is, however, cer- 
tain: In adults fatal bovine infection, if it does occur at all, is so rare 
that it is of no significance from any standpoint. Indeed, only in 
children under five years of age are bacilli of bovine origin apt to cause 
disease. 

Bovine tubercle bacilli, when found in humans, are always 
“zoogenetic.” If they were ‘“‘anthropogenetic’’—transmitted from 
man to man—the proportion of humans with bovine infections would 
be about the same in all organs. Bushnell’ suggests that infection 
with human bacilli is more likely to occur because of sufficiency of 
opportunities through contact with tuberculous persons, and for this 
reason it occurs early in life. The child is thus immunized against 
infection with bovine bacilli. If this immunization were not so wide- 
spread, infection with bovine bacilli would be more common. 

Virulence of Bovine Bacilli in Human Beings.—There appears to be 
some good and valid evidence to the effect that when a human being 
is infected with bovine tubercle bacilli, the disease produced is likely 


1 Lancet, 1915, 1, 1275. 

2 British Med., Jour., 1914, 1, 125. 

3 The Causes of Tuberculosis, London, 1917, p. 657, 
4 Epidemiology of Tuberculosis, p. 180, 


POISONS PRODUCED BY THE TUBERCLE BACILLI 30 


to run a favorable, and even a benign, course; only rarely is death 
caused by these microdrganisms. We know that it is the pulmonary 
form of tuberculosis which is fatal; while tuberculosis of the glands, 
joints, and bones tends to recovery in the vast majority of cases. 
Similarly, tuberculosis of the serous membranes, notably the peri- 
toneum, often shows a tendency to recovery. We will see later on in 
this book that this is also true, to a certain extent, of the pleura. 
The meninges are an exception, for obvious reasons. Now, the peri- 
toneum is very frequently affected by bovine tubercle. Moreover, 
tuberculosis of the cervical and thoracic glands is very common among 
children, yet the tuberculosis mortality among them is very low. 
This disease, in its various forms, kills less between three and twelve 
than at any other age period. Moreover, it has been found that in 
many instances caseous tissue obtained trom tuberculous glands, while 
showing the presence of acid-fast rods, fails to infect animals when they 
are inoculated. It has thus been suggested that these mild bovine 
infections of the cervical, mesenteric and thoracic glands, while in 
themselves harmless, nevertheless confer immunity to the organism 
which may last for life, and for that reason adults are safe against 
infection by human tubercle bacilli. We shall revert to this point 
later on. 


POISONS PRODUCED BY THE TUBERCLE BACILLI. 


When tubercle bacilli enter the human body they do harm in 
various ways. Locally, they destroy the tissues in which they have 
settled, producing coagulation necrosis, ete., which will be discussed 
later on. By their proliferation they also produce general disturb- 
ances in the functions of the invaded body which can only be explained 
as caused by some poison liberated by the bacilli. The nature of these 
poisons is obscure at present, although strong efforts have been made 
to ascertain all the facts in this respect. 

When dead tubercle bacilli are injected subcutaneously into the 
healthy animal, a distinct inflammation is produced at the site of the 
inoculation, frequently followed by suppuration. It is immaterial 
whether the bacteria have been killed by chemicals or by heat, the 
result is the same in either case. When dead tubercle bacilli-are 
injected intravenously into rabbits, provided a sufficient quantity 
is employed for the purpose, a proliferation of tissue in the lung is 
produced similar to that of tubercle, containing, as it does, giant 
cells which may caseate. After intratracheal insufflation, tuberculous 
nodules with epithelioid and giant cells are produced. 

On the other hand, when fluids containing the products of the metab- 
olism of tubercle bacilli are injected in very large doses into normal 
and healthy animals, no toxic effects are produced. 

These and other facts tend to show that the effects of the bacilli 
on the animal body are not due to mechanical irritation produced 


J 


36 THE TUBERCLE BACILLI 


at the site of the inoculation, but are the result of the liberation of 
toxic matter which acts both locally, producing coagulation necrosis, 
and generally, producing fever, etc. We know this, but attempts to 
isolate a true toxin from tubercle bacilli have utterly failed, and with the 
intensive studies that have been made during the past thirty-five years 
along these lines, we have not yet been able to clearly define the tuberculous 
poisons. ‘They appear to be part and parcel of the living protoplasm 
of the tubercle bacilli, and are liberated only after the latter have been 
destroyed. In other words, the tubercle bacilli belong to a group of 
macrodrganisms which do not secrete soluble toxins, but nevertheless pro- 
duce general effects on the body which they invade; their deleterious 
effects are the result of the action of endotoxins. 

Tuberculin.— Koch was the first to discover that when dead tubercle 
bacilli are injected in large quantities into tuberculous animals, death 
is caused; when small doses are injected, only a slight reaction is 
caused at the site of the inoculation, which soon heals. On repeated 
inoculations he observed improvement in the condition of the sick 
animal. On these experimental findings he based his suggestion for 
the use of tuberculin as a diagnostic and therapeutic agent in tuber- 
culosis. 

Tuberculin consists mainly of the culture fluid in which the bacilli 
have grown, of disintegrated bacilli, or extracts of their protoplasm, 
or both. As originally prepared by Koch, the following process is 
pursued: 

Tubercle bacilli are cultivated on bouillon made from fresh veal 
to which 1 per cent of dried peptone, 0.5 per cent of sodium chloride, 
and 5 per cent of glycerin are added. Within six to eight weeks of 
luxuriant growth at 38° C. the culture is poured into an evaporating 
dish, placed on a water bath, and evaporated to one-tenth the original 
volume, and any remains of bacilli are removed by filtration; con- 
taining 50 per cent of glycerin, the resulting preparation is quite 
stable. 

It is thus clear that tuberculin is not a true toxin, nor is it a pure 
endotoxin; but a 50 per cent glycerin solution of the products of 
macerated tubercle bacilli in the culture fluid which are not destroyed 
by heat, and also any portion of bacilli which remains in the solution, 
or both. 

Ever since the introduction of this original tuberculin, many other 
methods of preparation have been devised by Koch himself and others, 
but all have shown that the active principle is practically the same. 

The Action of Tuberculin.—There are differences of opinion as to 
whether tuberculin depends in its action on a certain chemical prin- 
ciple, or on several chemical substances. In fact, the chemical com- 
position of this preparation is obscure. Some have suggested that the 
active principle is a protein, or albumose. Klebs, Levene, and others 
believe that they have isolated various active principles; some have 
even obtained typical tuberculin reactions with these substances. 


POISONS PRODUCED BY THE TUBERCLE BACILLI of 


But, as will be shown when discussing the tuberculin reaction, any 
protein inoculated into a tuberculous individual produces practically 
the same effects—tuberculosis being invariably accompanied by an 
altered reactivity to these substances. It can be said emphatically 
that, at the present state of our knowledge, we are in the dark as to 
the active principle of tuberculin. 

Healthy animals bear the injection of tuberculin in large doses 
without any harm; the same is true of healthy human beings. Koch 
injected into his own body 0.25 cc of tuberculin and suffered from a 
severe reaction; after his death an autopsy showed that he had suf- 
fered from extensive pulmonary tuberculosis. On the other hand, 
Hamburger administered as much as 500 mgs. of tuberculin into 
non-tuberculous infants and children without producing the slightest 
local, or general, reaction. Clinical experience among human beings, 
as well as in cattle—in which it is easy and feasible to determine by 
autopsy whether there are tuberculous lesions—has shown that a 
reaction after a large dose of tuberculin in an apparently healthy 
person is conclusive proof of an existing tuberculous lesion some- 
where in the body. We shall show later on that this is true of the 
vast majority of people in civilized communities, and therefore reac- 
tions to large doses of tuberculin are of very little value to the clinician 
who looks for active tuberculosis. 

The reason why tuberculin is harmless in healthy organisms, and 
produces such a pronounced reaction when injected into tuberculous 
organisms, is not clear. Various theories have been advanced to 
explain it. The most widely accepted explanation is that of Wolff- 
Eisner. He assumes that tuberculous infection produces specific anti- 
bodies in the tissues which break down the tuberculin molecule, just 
as the digestive enzymes break down certain albumin molecules pro- 
ducing innocuous, and highly poisonous, albumoses. The antibody 
which acts in this manner he calls tuberculolysin. In non-tuberculous 
organisms there is no tuberculolysin, and when tuberculin is injected 
it circulates within the juices, producing no toxic effects, and is finally 
eliminated, like other harmless foreign proteins. In the tuberculous 
organism the tuberculin comes in contact with the lysin, is broken 
up, and liberates a toxic substance which produces the reaction. 

Phenomena of Hypersensitiveness.—When a rabbit is infected with 
tubercle bacilli, and four weeks later 0.1 to 0.3 ce of tuberculin is 
injected subcutaneously, the animal succumbs within six to twenty- 
four hours. Koch found that in animals infected eight to ten weeks 
previously 0.01 ¢ ¢ of tuberculin is sufficient to cause death. Injec- 
tions of very small doses into tuberculous animals produce only a more 
or less severe reaction—fever, loss of weight, ete. This is obtained 
with injections of either living or dead tubercle bacilli. 

When repeated small doses of tuberculin are injected, certain 
phenomena are observed which are not unlike those obtained after 
the injection of other foreign protein substances into an animal. 





38 THE TUBERCLE BACILLI 


The tuberculin reaction is evidently a manifestation of tuwherculo-protein 
hypersensitiveness. Some authors have, indeed, been inclined to 
ascribe the reaction to tuberculin to the action of the non-specific 
substances, glycerin, proteins, extractives, etc., contained in the 
tuberculin, and have argued that the reactions to repeated inocula- 
tions are anaphylactic phenomena. Perhaps the fact that the usual 
dose of tuberculin does not contain enough of foreign proteins dis- 
proves this contention, and shows that there must be some specific 
substances which are active in this regard. But this has not been 
proved conclusively. 

Theoretically, it would be expected that tuberculin, provoking the 
same phenomena in the animal body as the living tubercle bacilli, 
should also have an immunizing effect. But, so far, nobody has been 
successful in an attempt at immunization of the body with dead 
tubercle bacilli, or any part of the culture in which they grow. More 
satisfactory results have been obtained infecting animals with living 
bacilli. 

Tuberculin hypersensitiveness differs from anaphylaxis by the fact 
that in normal animals tuberculin may be injected in large or small 
amounts, at long or short intervals, without producing hypersensi- 
tiveness, and attempts at passive transference of tuberculin hyper- 
sensitiveness have led to doubtful results. Baldwin has been unable 
to produce transference, or passive anaphylaxis, from tuberculous 
guinea-pigs to healthy ones, and also from rabbit to rabbit, and from 
rabbit to guinea-pig. From human to guinea-pig the results were very 
doubtful, but to rabbit, partly successful. But another difference 
between anaphylactic shock and tuberculin hypersensitiveness may 
be mentioned. The former phenomenon appears immediately after 
an injection, while in the latter they are delayed for many hours; in 
the former there is a marked reduction in the temperature, etc., while 
in the latter the contrary is true. 

Specificity of the Tuberculin Reaction—We have seen that tuber- 
culin produces obvious effects only in the infected organism. The 
question then arises whether the reaction it produces is strictly specific. 
Many workers have found that tuberculous animals react to, and may 
even be killed by, the injection of any foreign bacterial protein of non- 
tuberculous origin in the same manner as by tuberculin. In human 
beings there was also found hypersensitiveness to non-tuberculous 
extracts from bacilli closely resembling the hypersensitiveness induced 
by tuberculin. Even the cutaneous tuberculin reaction can be pro- 
duced by non-tuberculous toxins inoculated in the same manner as 
tuberculin is applied in the von Pirquet and other tests. 

The changes in reactivity to tuberculin may be induced by non- 
tuberculous proteins and toxins. The general reaction, the fever, with 
concomitant subjective symptoms, such as headache, anorexia, ete., 
also the local reaction at the site of the inoculation, and finally even 
the so-called “fecal reaction” manifesting itself in the tuberculous 


POISONS PRODUCED BY THE TUBERCLE BACILLI 39 


lesion, have all been produced by non-tuberculous substances. More 
recently R. Schmidt! found that parenteral milk injections are often 
followed in tuberculous subjects by general, and focal reactions which 
cannot be distinguished from those produced by tuberculin. On 
the other hand, tuberculin has been known to produce these reactions 
in patients suffering from leprosy, syphilis, etc. The suggestion that 
this does not militate against the specificity of the tuberculin reaction, 
because these diseases may be combined with tuberculosis, does not 
explain every case. 

It has also been found by Mettetal,? and others, that individuals 
who react to tuberculin also react in.almost the same fashion to saline 
solutions, which would indicate that it is not necessarily the specific 
bodies in the tuberculin which are responsible for the fever, malaise, 
ete. At any rate, tuberculin is not the only substance that produces 
these phenomena in tuberculous individuals. 

Autopsy control has not cleared up the problem. There have been 
reported cases in which a positive reaction was obtained during life, 
but no tuberculous lesions could be discovered on careful dissection 
of the body after death, and the reverse. In cattle it was found that 
only 85 to 90 per cent of those reacting to tuberculin show tuberculous 
changes on dissection after slaughter, while 10 per cent of those which 
do not react show tuberculous changes in some ergans. ‘These facts 
have important bearings on the problems presented by tuberculin as 
a diagnostic agent and will be more fully discussed later on. 

Another problem arises when changed reactivity to tuberculin is 
found. Does it invariably indicate that the body is at the time har- 
boring living and virulent tubercle bacilli? Do individuals who have 
at one time passed through a tuberculous infection, but in whom 
the lesion has completely cicatrized, also show hypersensitiveness to 
tuberculin? To the first question we have a positive answer: Many 
healed, cicatrized, and calcified tuberculous lesions have been found 
to harbor virulent bacilli, as has been proved experimentally. These 
bacilli are, in fact, responsible for acute exacerbations observed in quies- 
cent and latent tuberculosis; they may also be held responsible for 
the onset of the average case of phthisis in adults, as will be shown 
elsewhere. But what is of more importance is whether, once acquired, 
the tuberculin hypersensitiveness remains throughout the life of the 
individual. ‘This is a problem which has not yet been investigated 
to an extent as to warrant a positive answer. 

Outside of such theoretical considerations, these problems have 
great practical bearings on the utility of tuberculin as a diagnostic 
agent, which is discussed in Chapter XIX. 


1 Deutsch. Arch. f. klin. Med., 1920, 131, 1. 
2 Valeur de la tuberculine dans la diagnostic de la tuberculose de la premiére enfance, 
Thése de Paris, 1900. 


GPA LE Rae 
TUBERCULOUS INFECTION. 


The Problems of Infection.— With the discovery of the tubercle 
bacillus in 1882 it was at once concluded that practically all the 
problems of phthisiogenesis had been settled. ‘The infective agent, 
the bacillus, enters the human body, implants itself in some tissue; 
by its growth and metabolic processes it produces toxic symptoms 
and, causing caseation and liquefaction, destroys vital organs, ete. 
With this knowledge, it was thought that the prevention of the disease 
had been reduced to simple principles: The destruction of the bacilli 
wherever found, and the prevention of their entry into the human 
body, when attempts at their destruction fail for any reason. 

To destroy the bacilli it was necessary to ascertain all the places 
where they are found in Nature. This was apparently an easy matter. 
We know that the tubercle bacillus is a strict parasite, living and 
multiplying only in the human and animal body. Investigations by 
Sander tend to show that, within certain limits, they can proliferate 
on vegetable media during the hot summer months, but it is problem- 
atical whether this mode of life explains any infection in man. After 
the facts gathered by careful investigators are taken into considera- 
tion, there is no doubt that the only suitable soil for life, growth and 
multiplication of this bacillus is the animal body, and that the secre- 
tions and excretions of diseased persons and animals are the only 
means of disseminating the disease. 

We have shown that bacteriologists have distinguished at least 
four main types of pathogenic tubercle bacilli: the human, the bovine, 
the avian, and the reptilian. Practical experience has shown that the 
last two types, those of birds, and of cold-blooded animals, play no 
role in the epidemiology of tuberculosis in human beings, at least 
not a very significant réle. There are consequently left the human 
and bovine types to be considered as etiologically important in tuber- 
culosis in human beings. 

Careful investigations by Theobald Smith, William H. Park, A. S. 
Griffith, Fraser, The British Royal Commission, The German Imperial 
Health Board, and others, have shown that more than 99 per cent of 
phthisis in adults, and about 85 to 90 per cent of serious tuberculous 
disease in children are due to the human type of bacillus; that the 
bovine type is found in about 10 per cent of tuberculosis in children, 
and in pulmonary tuberculosis in adults this type is so exceptional 
as to make each case worthy of careful reporting. It also appears 


MUTATION OF THE TYPES OF BACILLI 4] 


from the evidence thus far gathered that tuberculosis in children due 
to bovine bacilli is mostly of the milder forms of the disease—surgical 
tuberculosis, of the glandular systems, especially of the thoracic and 
the abdominal glands, of the joints, bones, and skin. In other words, 
the diseases caused by the ingestion of bacilli with milk from tubercu- 
lous cows are not of great significance, except perhaps in infants, when 
compared with the immensity of the problems presented by infections 
with the human type of bacilli, causing phthisis in adults, and most 
cases of fatal tuberculosis in infants. 

For these reasons, some authors have stated that bovine infections 
may be disregarded; only infection with bacilli acquired through the 
entry of tubercle bacilli which have been incubated, so to say, in 
tuberculous human beings, is to be combated, if phthisis is to be eradi- 
cated at all. The corollary to be drawn is that the sources of the 
tubercle bacilli are mainly human consumptives. 

Mutation of the Types of Bacilli.— Further study has, however, 
complicated this problem. It has been suggested by many authors, 
notably Orth,! Rabinowitsch, Beitzke, Much, and others, that bovine 
bacilli, remaining in the human body for a long time, and adapting 
themselves to the surroundings, may acquire the characteristics of the 
human type, a kind of biological transformation of type, or mutation. 
It isclear that in our attempts at eradication of phthisis this problem 
is of immense importance. The 10 per cent, or more, of children in 
civilized countries who are infected during childhood with milder 
forms of tuberculosis thus harbor the bovine bacilli within their 
bodies for many years, during which time they adapt themselves to 
the surroundings within the human body, and when they cause phthisis 
in the adult we find them with the characteristics of the human type. 

In support of this assertion it was shown that very often “atypical”’ 
bacilli are found in cases of tuberculosis; they are microérganisms 
which cannot be classed with either the human, or the bovine type. 
They have been called “transitional” types; types which may have 
been originally bovine, but after sojourning in the human body for 
some time, are on the way to acquiring traits of human bacilli. 

The British Royal Commission says in this connection that they 
“are inclined to regard transmutation of the bacillary type as exceed- 
ingly difficult, if not impracticable, of accomplishment by laboratory 
procedure; though in view of certain instances in which we obtained 
from one and the same human body both types of bacillus, we are not 
prepared to deny that transmutation of one type into another may 
occur in Nature.” ‘‘ Direct experiment has not succeeded in proving 
that a tubercle bacillus of given type can be transformed into one of 
another type by being made to reside in the body of a new host in 
which tuberculosis, when it occurs naturally, is caused by the latter 
type of bacillus,’ says Cobbett.? Arloing, Marcus, Rabinowitsch, 





1 Drei Vortrige tiber Tuberkulose, Berlin, 1913. 
2 The Causes of Tuberculosis, London, 1917, p. 368. 


42 TUBERCULOUS INFECTION 


Sorgo, Musemeier, Dammann, and especially Léwenstein,! claim to 
have been able to produce changes in the morphological and cultural 
characters, and in the virulence of bacilli by passage through various 
animals, or cultivating them in different media. But Park and Krum- 
wiede? say: “We have carefully examined the reports of numerous 
workers on this point, and cannot admit that the evidence for the trans- 
formation of type is complete.”’ Theobald Smith, after studying the 
evidence, also arrives at the conclusion that “in general the results of 
these passages have been negative, so far as any recognizable modifi- 
cation of type is concerned.” Park’s suggestion that the change in 
type observed after passing through a series of animals is due to addi- 
tional bovine infection has a great deal in its favor. As has been shown 
by Cobbett,’® the more the conditions for carrying out such researches 
are made to approach the ideal, the rarer become the instances of 
apparent modification of type. Cases in which both types were found 
in human beings have been reported. 

We are therefore justified in concluding with Park and Krumwiede 
that “the two types are probably different due to residence in different 
hosts over long periods of time, and as such are stable. The evidence 
of rapid change is incomplete and inconclusive.” In the human 
disease the stability of type is apparently beyond question. Some 
cases have been followed for long years and the type of the bacillus 
has been found to be unaltered. Weber and Steffenhagan have fol- 
lowed for ten and a half years a case of surgical tuberculosis and always 
found bovine bacilli, without changing their typical characteristics. 

However, the weight of evidence is in agreement with Cobbett# 
to the effect that if transformation of type does not occur in our 
laboratory experiments which, prolong them how we will, are neces- 
sarily limited in time, it does not follow that an exceedingly slow modi- 
fication of type does not take place when a suitable change of host 
occurs, as for example when bovine tubercle bacilli take up their resi- 
dence for several generations in man, pig, or horse. Such a change is 
perhaps dimly indicated in some of the experiments with viruses of the 
bovine type taken from these species. This slow alteration, which 
appears probable (though the actual evidence for its existence is very 
slender) is, if it occurs at all, of a magnitude altogether different from 
that of the more or less sudden and complete changes of type which 
have appeared in some of the passage experiments. But such slow 
changes hinted at here are of little more than theoretical importance. 

On the other hand, Brownlee,’ taking into consideration that the 
frequency with which bovine tuberculosis occurs decreases with age 


1 Vorlesungen tiber Tuberkulose, Jena, 1920, p. 80. 

2 Tr. Sixth Ann. Meet. Nat. Assn., Study and Prevent. Tuberc., 1910, p. 322; Jour. 
Med. Research, 1911, 20, 313; 1912, 22, 109. 

3 Loc. cit., p. 367. 

4 Tbid., p. 369. 

5 An Investigation into the Epidemiology of Phthisis in Great Britain and Ireland, 
Part III, London, 1920, p. 56. 


THE CHANNELS OF ENTRY OF THE TUBERCLE BACILLI 43 


(see p. 33), 1s inclined to the opinion that “the evidence strongly 
suggests that in the human laboratory a change from the bovine to 
the human type takes place. This is rendered more probable by the 
fact that when bovine bacilli have been injected into horses and dogs 
changes in the character of the organisms associated with the loss of 
some of the characteristics peculiar to the bovine type of organisms 
have been observed.” He also suggests the possibility that bovine and 
human tubercle may be modifications in two directions of an organism 
standing somewhere between. It is also possible that the organism 
may have an independent existence, that is to say, may live sapro- 
phytically outside the body under conditions not at present understood. 
A well known example of this kind is the streptococcus, which is a 
notoriously delicate organism when grown under laboratory conditions, 
but which is ubiquitous. 

The weight of evidence is, however, in favor of human phthisis being 
due almost exclusively to human bacilli, and that infection during 
childhood with bovine bacilli cannot be held responsible for phthisis 
in the adult, because, so far, it has not been proved that mutation of 
one type into another takes place. 

The source of the bacilli causing phthisis in the adult, and serious or 
fatal tuberculosis in infants or children, appears to be the tuberculous 
man who expectorates myriads of bacilli fit for entering healthy persons 
and causing disease. 

The Channels of Entry of the Tubercle Bacilli.—In our attempts at 
prevention of tuberculous disease we must be first definitely informed 
on the channels through which these microérganisms enter the human 
body. ‘To the average person, lay or medical, who has informed him- 
self from current popular literature, this question has been answered 
satisfactorily. If the bacilli are derived from human sources, they have 
usually been inhaled, and exceptionally ingested; if from bovine 
sources, they have been ingested. 

But it may be stated without fear of meeting contradiction from 
competent sources that this problem has not yet been solved to the 
satisfaction of all who are entitled to an opinion. Romer,! one of the 
most active experimental workers in the field of tuberculosis, and one 
of the best qualified to speak authoritatively, says that none of the 
giwen channels of entry of the tubercle bacilli rs alone sufficient to adequately 
solve all the problems presented by tuberculous infection. 

Obviously there are four portals of entry which are to be mentioned 
as possible: 

1. Inoculation into the skin or mucous membranes. 

2. Inhalation through the respiratory passages, or aérogenous infec- 
tion. 

3. Ingestion through the digestive tract, intestinal infection. 

4. Germinative, or placental infection, the bacilli being derived from 
the parents before the birth of the individual. 

1 Handb. d. Tuberkul., 1, 247. 


44 TUBERCULOUS INFECTION 


Inoculation and Contact Infection Considering the ubiquity of 
the tubercle bacilli, the skin should be the most common channel of 
entry of these germs into the body. The transfer of germs from hand 
to hand, and from hand to mouth, is very difficult to avoid when it is 
borne in mind that every individual living in a civilized community 
must come in contact with tubercle bacilli in his daily routine life. 
Palmer! enumerated the chances of acquiring a communicable disease 
by contact and he mentions one hundred and nineteen points of con- 
tact, from touching of door-knobs, faucets, various eating utensils, and 
money, to handshaking, receiving newspapers, touching telephone 
directories, saliva-moistened street car transfers, etc. J. B. Rogers? 
found experimentally that such objects as gauze used to cover the 
mouth when coughing, pillow cases used twenty-four hours, patient’s 
hand, spoons used by patients, magazine covers picked up indiscrimi- 
nately from the wards, and door-knobs frequently handled by patients, 
are contaminated by virulent tubercle bacilli. On the other hand, 
other workers along these lines have found that the dangers of infection 
in this manner are rather remote.* 

Inoculation of tubercle bacilli into the skin and mucous membranes 
may cause disease. This has been proved beyond any doubt experi- 
mentally and clinically. Inoculated tuberculosis is most virulent on 
virgin soil, as is observed in animal experimentation, and in infants 
who have thus been infected during ritual circumcision as practiced 
by orthodox Jews, of which many cases have been reported, notably 
by Arluck, Bernhardt, Winocouroff, Holt, and others. Local tuber- 
culous lesions have also been observed to result from infections acquired 
by surgeons, anatomists, pathologists, veterinarians, butchers, ete. 
But there are more curious ways in which this mode of infection has 
been observed to occur. Deneke, Moro, and others, report cases in 
which children have been inoculated with tubercle bacilli while break- 
ing sputum receptacles. There have also been reported infections 
acquired while tattooing (Ernst), while piercing the ears in girls, the 
needle being moistened with the saliva of a tuberculous individual 
(Grosser, Grossmann, Patzold), by hypodermic needles, ete. 

Inoculation of tubercle bacilli into susceptible animals, and human 
infants, produces a fatal bacteremia, as a rule, but in adults only a 
local lesion at the point of entry of the germs results. The reasons for 
these differences will be discussed later on. On the other hand, when 
considering cutaneous skin affections, such as the various clinical 
forms of lupus, or the so-called tuberculides, it must not be hastily 
concluded that they are invariably acquired by inoculation. As will 
be shown later on, while discussing hematogenous and lymphogenous 
infection, the germs are usually brought there by the blood or lymph 
stream. 

1 Am. Jour. Pub. Health, 1919, 9, 267. 


2 Am. Jour. Pub. Health, 1920, 10, 345; Jour. Am. Med. Assn., 1920, 75, 1690. 
3 See Brown, Petroff and Pasquera: Am. Rey. of Tuberculosis, 1919, 3, 621. 


IMMUNITY OF THE SKIN 45 


Immunity of the Skin.—Contact infection, even though it may 
occur, is not of great importance in phthisiogenesis. Of all the organs, 
the skin appears to be the least vulnerable to tuberculosis, as has been 
shown by Lewandowsky.! Its low temperature, as well as its chemical 
and anatomical structure appear to offer unfavorable conditions for 
the growth and proliferation of tubercle bacilli; in fact, there is strong 
evidence that it offers vigorous resistance to tuberculous infection. 
Facts gathered from comparative pathology show that animals known 
to be very susceptible to tuberculosis have only rarely skin lesions. 
Tubercle bacilli may penetrate the normal animal skin and produce 
visceral tuberculosis without leaving any traces on the skin itself. 
Although Takeya and Dold state that they could always find tuber- 
culous changes at the point of entry, C. Friinkel, Courmont and André, 
Lesieur, Babes, and others, report the contrary. Babes and Friinkel 
found tubercle bacilli in the lymph vessels of the subcutaneous tissues 
four to forty-eight hours after rubbing the germs into the skin of 
animals, which shows clearly that they may penetrate the skin without 
damaging it. 

The immunity of the human skin is also evident from the fact that, 
though exposed to infection more than any other organ, it is but 
rarely tuberculous. Indeed, tuberculous skin diseases are very rare 
in phthisical patients who can hardly avoid inoculation. It is the 
consensus of opinion that the various tuberculides seen in tuberculous 
patients, especially children, such as the papulo-necrotic tuberculides, 
lichen scrofulosorum, erythema induratum, sarcoid, etc., are mani- 
festations of reactions of skin hypersensitiveness of tuberculous indi- 
viduals, brought about by dead bacilli carried by the blood and lymph 
streams. Other tuberculous skin diseases, such as the various forms of 
lupus, etc., even when due to local infection, as is the case with tubercu- 
losis verrucosa cutis, etc., may disfigure, but they nevertheless run 
a mild course, hardly ever leading to fatal termination by extension 
ot the disease to visceral organs. Moreover, the skin lesions them- 
selves remain localized for many years without showing any pronounced 
tendency to extension. When compared with the skin lesions ot ter- 
tiary syphilis, which tend to spread and destroy, it is clear that tuber- 
culosis of the skin is a rather mild disease. ‘‘The skin is not a culture 
medium for the tubercle bacillus, it does not permit it to grow and 
proliferate,’ says Lewandowsky. Microscopically, this is confirmed 
by the paucity of tubercle bacilli in most tuberculous lesions of the 
skin. It must also be mentioned in this connection that various 
investigators have found that a large proportion of skin lesions are 
caused by bovine tubercle bacilli, which were isolated in pure culture 
from lesions of certain forms of lupus vulgaris. 

Available evidence thus tends to show that infection through the 
skin is hardly of any importance in the etiology of tuberculosis of 


1 Die Tuberkulose der Haut, Berlin, 1916, p. 32, 


46 TUBERCULOUS INFECTION 


visceral organs, notably the lungs. As will be shown later on, even 
in cases in which a tuberculous skin disease terminates fatally with 
symptoms of miliary tuberculosis, it is usually due to a reactivation 
of dormant lesions in the glands, or lungs. 

Infection by Inhalation of the Bacilli.—That the virus of tubercu- 
losis is inhaled with the inspired air has been asserted for centuries 
by physicians, and Villemin suggested this mode of infection after 
his experimental investigations. But Koch and his pupil Cornet! 
were the first to prove that dust containing tubercle bacilli derived 
from desiccated sputum is highly infectious to guinea-pigs. Cornet’s 
experiment with dried sputum scattered over a carpet on which the 
animals were compelled to live while the carpet was often swept with 
a stiff broom, has remained classical, and is often quoted as proving 
conclusively the dangers lurking in dried sputum in the average dwell- 
ing inhabited by careless consumptives. On the basis of such experi- 
ments rested the entire inhalation hypothesis of tuberculous infection. 

The fact that diffuse daylight, especially sun-rays, kills tubercle 
bacilli, and soon renders them avirulent, would largely exclude infec- 
tion through sputum deposited in the street and in large, bright sunny 
rooms. But the average consumptive, derived as he is from the poorer 
strata of population, and living in a squalid dwelling, lacking sufficient 
light, may deposit sputum which retains its virulence for a long time. 

Many valid objections have been raised against the theory that 
desiccated tuberculous sputum is the main source of infection in man. 
Fliigge,? and many others, have shown that in the ordinary course 
of human events things are not as simple as stated by Cornet and 
Koch. The experiments with the carpet are not altogether analogous 
to the conditions found in human dwellings, and by no means prove 
that infection is acquired mainly through the inhalation of dust laden 
with dried tuberculous sputum. Such large quantities of sputum as 
were used by Cornet in his experiments on guinea-pigs are exceedingly 
rarely, if ever, found in the most squalid of dwellings. It is also 
doubtful whether dust laden with virulent tubercle bacilli is often 
raised to the height of the human head to be inhaled in sufficient 
amount to infect, even while the floor is being swept. 

In fact, further investigations by Fliigge, Neisser, Kohlisch, and 
others have not yielded the same results as those reported by Koch, 
Cornet, and their followers. It was found that in houses inhabited 
by consumptives the sputum deposited on the floors is not often 
perfectly dried and thinly pulverized, capable of rising with the dust 
to the height of five or more feet from the ground. Moreover, con- 
ditions in unsanitary homes are, as a rule, not conducive to drying 
the sputum soon after it has been eliminated by the consump- 
tive. And if it takes time to dry, it must be remembered that the 
bacilli lose their virulence within ten days, owing to putrefactive pro- 


1 Verhandl. Berl. med. Gesellsch., 1899, 30, 91. 
2 Ztschr. f. Hyg. u. Infectionskrankh., 1909, 30, 107, 


INFECTION BY INHALATION OF THE BACILLI 47 


cesses on the floors of filthy houses, and the diffuse light which acts 
during the day, or artificially, during the night. It is also noteworthy 
in this connection that in the average house there are no air currents 
strong enough to raise the dust to the height of about five feet. 

It may seem incredible, vet it is a fact that it is exceedingly rare 
to find a house where proper precautions are taken as to expectoration 
in which the collected dust shows virulent tubercle bacilli. Even in 
houses inhabited or frequented by consumptives—sanatoriums, dis- 
pensaries, railroad stations, factories, cars, ete.—no dust containing 
virulent tubercle bacilli has been found in most cases investigated. 
Thus, K6hlisch! could not infect guinea-pigs, which are very suscepti- 
ble, with dust collected in houses inhabited by consumptives, and he 
concludes that it has no significance in the origin of tuberculous disease. 
Wagner collected dust in a sanatorium at Zurich, in such places in 
which the air stream could have dispersed it, and injected it intra- 
peritoneally into guinea-pigs and found that in only 3.5 per cent of 
cases did infection take place. Brown, Petroff, and Pasquera report 
about dust collected by a vacuum cleaner from a large rug in the living 
room of the Trudeau Sanatorium. It proved negative when injected 
into a guinea-pig. The same result was obtained with the dust from a 
room in the infirmary occupied by a patient with numerous tubercle 
bacilli in the sputum and a cough so explosive that the mouth was 
rarely covered. They also collected dust before the daily cleaning by 
swabbing with sterile swabs the bed, tables, chairs, bed frames, corners 
of the rooms and walls near the patient. The swabs were washed in 
sterile broth, the washings treated with normal sodium hydroxide, 
incubated for half an hour, then neutralized with normal hydro- 
chloric acid, centrifugalized, and the sediment divided into three por- 
tions. One was inoculated into gentian violet media, another stained 
on a slide for microscopic examination, and the third inoculated sub- 
cutaneously into the inguinal region of guinea-pigs, two for each swab. 
In all twenty-four animals were used. All the slides were negative as 
regards tubercle bacilli, and none of the twenty-four animals showed 
any signs of tuberculosis when carefully examined at the autopsy. 
The dust in the rooms inhabited by two tuberculous patients outside 
of the sanatorium was also found negative for tubercle bacilli. The 
same was true of the mouth pieces of the telephone used by patients 
at the sanatorium. Dust collected in the streets hardly ever shows 
the presence of living and virulent tubercle bacilli. 

It thus appears that the hypothesis of pulmonary tuberculosis 
resulting from infection brought about by inhalation of bacilli entering 
the respiratory passages with the inhaled air during respiration is 
not conclusively proved. Those interested in this particular phase of 
tuberculous infection may find ample data in Calmette’s? most recent 
work. 


1 Ztschr. f. Hyg. u. Infectionskrankh., 1916, 81, 203. 
2 L’infection bacillaire et la tuberculose, Paris, 1920, pp. 127-144, 


4S TUBERCULOUS INFECTION | 


Droplet Infection.—It is obvious that though infection through 
the inhalation of dust containing desiccated tuberculous sputum is 
undoubtedly possible, this is not the only, or the most common, mode 
of spontaneous infection of human beings under “natural conditions,” 
and many have maintained that in the vast majority of cases infec- 
tion is accomplished directly from one person to another. The moist 
droplets eliminated by consumptives while speaking, and especially 
while coughing and sneezing, may be inhaled by persons who happen 
to be in their proximity. Fliigge! and his followers, who have done 
considerable experimental work along these lines, are satisfied that 
under natural conditions the dissemination of tuberculosis from man 
to man, ‘‘droplet infection,” is the most common mode. 

Careful research has shown that the air exhaled by consumptives 
during ordinary and quiet breathing is free from tubercle bacilli, 
but the moist droplets eliminated from the mouth while talking, 
coughing, sneezing, etc., do often contain tubercle bacilli which may 
remain floating in the air for some time. Indeed, it has been found 
that the Bacillus prodigiosus may thus float in the air for five hours. 
In various parts of a large hall Laschtschenko? placed Petri dishes 
containing culture media. He then washed his mouth with a suspen- 
sion of Bacillus prodigiosus, a microdrganism which is not found 
naturally in the air, and which may be easily identified. Atter deliver- 
ing a speech, he proceeded to collect the dishes and placed them in an 
incubator. Many of the culture media in the dishes showed excellent 
growth of the bacteria. Gordon’ repeated this experiment and obtained 
the same results. 

The problems of droplet infection are many, and it may be said 
that no agreement has yet been arrived at by all who are entitled to 
an opinion. Experimentally it has been shown that when a tuberculous 
patient coughs at a cover-glass, bacilli are found on the slide in a vari- 
able proportion of cases. It seems that in order that the bacilli should 
be deposited on the cover-glass it must be held close to the mouth of 
the patient. Some authors found that while when held 40 to 80 em. 
away from the patient’s mouth 30 per cent of the cover glasses show 
tubercle bacilli microscopically; no bacilli are deposited when it is 
held one meter or more away from the mouth of the patient. Engel- 
mann showed that when the slide is held at the side of the patient’s 
face, negative results are obtained even when the distance is but 
30 em. from the patient’s face. In this country J. B. Rogers obtained 
positive results at a distance of fifteen inches, but Brown, Petroff and 
Pasquera met with failure while making somewhat similar experiments. 

Placing susceptible animals before consumptives is another experi- 
mental method. Fliigge immobilized guinea-pigs and had tuberculous 


1 Die Verbreitungsweise und Bekimpfung der Tuberkulose auf Grund experimenteller 
Untersuchungen, Leipzig, 1908. 

2 Ztschr. f. Hyg., 1899, 30, 125. 

§ Suppl. Ann. Report Med. Off. Loc. Govt. Board, 1902-3, p. 425. 


DROPLET INFECTION 49 


patients cough directly intotheirmouths. The pigsbecame tuberculous 
in 6 out of 25 cases. Moller had tuberculous patients cough at guinea- 
pigs daily for several weeks, and in 2 out of 14 cases was tuberculosis 
thus transmitted. 

These experiments were apparently more often positive than in the 
case of experimental infection with dust containing desiccated tuber- 
culous sputum, and Fliigge and his followers conclude that this mode 
of infection is the most important under natural conditions. 

But even these experiments are open to question. The animals 
were held tightly for hours, directly exposed to the faces of the con- 
sumptives who coughed directly into their open mouths. Such ex- 
posure never occurs in human beings, except perhaps in cases of 
tuberculous mothers holding their crying babies on their arms, and 
coughing directly into their open mouths, which may be observed now 
and then among certain classes, but after all cannot be considered 
very common. 

A somewhat analogous experiment among humans was made by 
F. Hamburger.! He placed a feeble-minded boy, aged nine years, in 
a room in which three tuberculous girls lived. Because of the mental 
state of the boy, the girls avoided him and never came into close 
contact with him. And he remained free from tuberculous infection, 
as shown by the negative tuberculin reaction, for seven months. On 
the other hand, in a room in which a tuberculous patient was harbored, 
four children, aged two, four, five and ten years respectively, were 
brought in. Within four weeks all the four children, who before coming 
into the room with the tuberculous patient were tuberculin negative, 
showed a positive reaction to tuberculin. A somewhat similar observa- 
tion was made by Hess in an infant asylum in New York City where a 
tuberculous nurse thus infected several infants in a ward in which she 
was stationed. 

Even conceding that droplet infection is an important mode of 
transmission of tuberculosis, it must be realized that it depends on 
many factors which are not always, or even often, operative. When 
a healthy person is at a distance of three feet from the coughing patient, 
the droplets will not reach far enough to become a possible infective 
agent, excepting perhaps when carried by air currents. Another 
important factor is the dose of the bacilli that may thus be inhaled. 
As has been shown elsewhere, small numbers of bacilli are easily taken 
care of by the human organism. It is also a fact that tubercle bacilli 
thus eliminated do not remain floating in the air for any length of time, 
but sink to the floor, where they are soon rendered innocuous, as was 
already mentioned. 

It is thus obvious that only when contact with the consumptive 
is very close, intimate, and prolonged, which in ordinary life occurs, 
as a rule, only in mothers with suckling infants, or between husband 


1 Wien. klin. Wchnschr., 1919, 32, 33. 


50 TUBERCULOUS INFECTION 


and wife, droplet infection may become a serious menace. And even 
in these cases there are natural safeguards. 

Considering the evidence thus far brought together at its face value, 
it appears that inhalation of dust containing tuberculous sputum, or 
of droplets expelled by consumptives while talking, coughing, and sneez- 
ing, may infect a healthy person, yet the evidence that these are the most 
frequent modes of the dissemination of tuberculosis 1s inadequate. 

From time immemorial physicians have attributed the transmission 
of infectious diseases to the inhalation of the virus. To the ancients 
“infection” meant everything that contaminates the air (Infection, 
from the Latin infectionem, infectus, or more exactly impregnated). 
This has notably been the case with the endemic diseases of childhood, 
and for a long time yellow fever, typhoid, typhus, malaria, relapsing 
fever, bubonic plague, ete., were all considered inhalation diseases, and 
proofs were at hand to substantiate these contentions. Recently more 
exact studies have shown conclusively in some, and with a high degree 
of probability in others, that they are altogether transmitted through 
the agency of certain insects. Indeed, physicians of a few generations 
ago drew analogies between tuberculosis and malaria, typhus, etc., 
showing that they were all caused by the inhalation of the virus. 

Natural Barriers against Inhalation Infection.— Notwithstanding the 
various disharmonies which may be found in the structure and 
functions of the human body, and which Metchnikoff has so cleverly 
enumerated in one of his books, the respiratory tract is provided with 
a most wonderful protective apparatus for the prevention of the 
entry and implantation of bacilli in the deeper respiratory passages. 
Indeed, no organ in the body, excepting the central nervous system, 
is fitted out with better safeguards in this regard. 

The bacilli cannot enter the lungs with ease. The nasal passages, 
mouth and throat act as excellent filters, detaining the inhaled dust. 
Even when some microdrganisms in the inhaled air pass all the bar- 
riers, the mucus secreted all along the tract, the ciliated epithelium, 
etc., soon remove them as foreign bodies, when necessary assisted by 
cough, which has the function of clearing the lungs. Investigations of 
normal lungs have shown that they are germ-free; animal inocula- 
tions made by F. Miiller, Goebel, Klipstein, Bartel, and others, have 
failed to reveal any pathogenic microérganisms, though Diirck found 
the contrary to be true. But in such cases it has been suggested that 
the germs reached the lungs shortly before death and could not be 
expelled, or destroyed by the dying tissues. The few bacteria which 
may remain within for any reason are, under normal conditions, well 
cared for by the extensive lymphatic apparatus which surrounds all 
the bronchi and bloodvessels, even the terminal bronchioles, and takes 
up bacteria, destroying them or at least rendering them innocuous. 

From animal experiments, conducted for years, Bacmeister! shows 


* 


1 Die Entstehung der menschlichen Lungenphthise, Berlin, 1914. 


NATURAL BARRIERS AGAINST INHALATION INFECTION 51 


that while tubercle bacilli are rarely found in the lungs of animals 
compelled to inhale dust containing the germs, he never observed 
that infection of the normal lung was caused in this manner, and he 
concludes that the bacilli must be hindered in their development, 
destroyed, or carried away from the lungs by the lymph and blood 
stream. There is no reason against the assumption that the normal 
human lung acts in the same manner, and that bacilli which may 
succeed in penetrating into deep air vesicles are removed or destroyed 
before they can gain a foothold and cause disease. 

It must, however, be borne in mind that dust of any kind may, and 
at times does, reach the lungs with the inspired air, as is evident from 
the large number of cases of pneumokoniosis of various degrees. 
Tubercle bacilli may likewise be brought there with the inspired air 
or with dust. But whether they cause disease in every case in which 
they reach the lungs is a disputed problem, the weight of evidence 
being against such a contention. Indeed, it has been proved that 
tubercle bacilli may remain alive and virulent in the tracheobronchial 
glands for years without causing disease, or even changes in the glands. 
Investigations by Bartel and Weichselbaum, Harbitz, and others, have 
shown that this is frequently the case, and it explains the latency of 
tuberculosis in many cases (see page 143). 

That tubercle bacilli on mucous membranes do not invariably 
cause disease is proved by another fact. These microdrganisms 
have been found on the mucous membranes of the nose, throat, and 
mouth of healthy individuals. Noble W. Jones' found them in the 
nasal cavities of healthy persons in the ordinary walks of life, espe- 
cially those who cared for consumptive patients. Strauss? found 
tubercle bacilli in the nasal cavities of healthy individuals living in 
houses inhabited by phthisical patients. Alexander* found them in 
very large numbers on the mucous membranes of patients suffering 
from ozena, but who had no symptoms or signs of tuberculosis. These 
facts, taken in connection with the fact that tuberculosis of mucous 
membranes of the pharynx, nose, and mouth is exceedingly rare even 
in consumptives, show that these structures possess a certain natural 
resistance against tuberculosis. That it is not solely due to the immu- 
nity acquired by previous tuberculous infection is shown by the fact 
that, as a primary infection, tuberculosis of these parts is exceedingly 
rare, though it must be admitted that while entering the body, by 
inhalation or ingestion, the bacilli must pass them and they have 
greater opportunities to implant themselves there than in the deeper 
respiratory passages. 

A lymphatic apparatus of normal structure and function evidently 
insures against the implantation and pathogenic action of all kinds of 
bacteria in the respiratory passages. Otherwise we would all succumb 

Med. Record, 1900, 58, 285. 


3 
2 Bull. de l’Acad. de méd., Paris, 1894, 32, 18. 
3 Berl. klin. Wehnschr., 1903, 40, 508. 


52 TUBERCULOUS INFECTION 


to various microbic diseases, including tuberculosis. It is only when the 
natural protective forces fail that tuberculous disease may be caused 
in this manner. 

On the other hand, it must be emphasized that the lungs are very 
much exposed to infection from the blood stream, and hematogenous 
infection may easily localize itself in these organs. The lungs are the 
first filter for everything that may be carried by the venous circulation. 
When the lymphatic apparatus is injured by anthracosis, which is 
very frequent to some degree in nearly all adult city dwellers, it is 
not capable of removing tubercle bacilli which may be brought to it 
with the blood stream. But here, again, it appears that persons suffer- 
ing from anthracosis, with but few exceptions, are no more liable to 
tuberculosis than others (see p. 132). In fact, coal miners are rela- 
tively immune. 

Difficulties in the Way of Establishing the Portals of Entry of 
Tubercle Bacilli.— The reasons why experimental investigations have 
failed to adequately solve the problems of the aérogenous etiology of 
phthisis are evident when we bear in mind that pulmonary tuberculosis, 
as met with in human beings, showing isolated foct which extend slowly 
downward in the lungs, never occurs spontaneously in animals; nor has 
it ever been induced artificially, or experimentally, im animals. 

Really active initial lesions in the human lungs have only rarely been 
encountered at necropsies. Most cases examined on the autopsy 
table are advanced, and it is very difficult, or impossible, to decide 
which was the initial lesion. Even the initial lesions, found in indi- 
viduals who died from causes other than tuberculosis, and reported 
by Schmorl,! Birch-Hirschfeld,? Lubarsch,* Beitzke,‘ and others, have 
not cleared up definitely the problem whether the bacilli were brought 
to the site of the lesion by the inspired air or the blood stream. It 
has, however, been found that even at that stage both the bronchioles 
and the bloodvessels were affected to such an extent that either, or 
both, could be considered the portal of entry. It is difficult or impos- 
sible to decide which is the initial lesion, even in experimental tuber- 
culosis. “The fixing of the portals by the so-called oldest lesion,” 
says Ravenel,® “is open to serious question. I have produced fatal 
pulmonary tuberculosis in monkeys by feeding, with very insignificant 
intestinal lesions. All the oldest lesions were located in the lungs and 
bronchial glands, yet the method of feeding largely precluded the 
possibility of the tubercle bacilli reaching the lung, except through the 
digestive tract.” This is well known to every observing clinician and 
pathologist. It is not the rule that the most extensive, perhaps the 
fatal, lesion was the first. Indeed, in most cases we find a healed or 


1 Miinchen. med. Wehnschr., 1902, 49, 1379. 
2 Deutsch. Arch. f. klin. Med., 1899, 44, 58. 

3 Virchow’s Arch., 1913, 218. 

4 Berl. klin. Wehnschr., 1909, 46, 388. 

5 Jour. Am. Med. Assn., 1916, 46, 613. 


HEMATOGENOUS INFECTION 53 


smouldering lesion in one lung, while the newer lesion, in the opposite 
lung, is progressive and destructive. Similarly, we meet with mild, 
perhaps almost healed, lesions in the lungs, while a secondary lesion in 
the kidneys, or some other visceral organ, is the most important in 
causing a fatal termination. We are not always sure in assigning the 
portal of infection to the small gland which is found to harbor an old 
tuberculous lesion. 

The fact that the regional lymphatic glands and lymph nodes are 
usually implicated at an early stage points to a hematogenous localiza- 
tion, but it may also be explained by the aérogenous hypothesis. 

It is obvious that the inhalation of the bacilli does not exclude 
hematogenous distribution and their final localization at some point 
distant from the point of entry. Ribbert, Bacmeister, Lubarsch, 
Ravenel, Theobald Smith, and others, have pointed out that micro- 
organisms brought into the bronchial tree by the inspired air may pass 
through the mucous membrane into the lung tissue without producing 
a visible lesion at the point of entry; pass along the lymphatics into 
the regional lymph nodes and from there carried by the blood stream 
into the pulmonary apices. But that this is in all probability rare, 
may be assumed when it is recalled that only few bacilli can reach 
the bronchi, and of these but few are allowed to pass through the normal 
mucous membrane of these tubes and the alveoli, and they are usually 
rendered innocuous by the protective properties and functions of the 
lymph and blood, as was just shown. 

Hematogenous Infection.— Many look at phthisis as hematogenous 
in origin: The tubercle bacilli are assumed to enter the body at any 
point, the respiratory or digestive tract, or even through the skin, 
and are carried by the blood stream until they reach a point where the 
tissues have a low power of resistance, an organ which offers a favor- 
able soil for the growth and action of these microbrganisms. Con- 
sidering the enormous frequency of pulmonary phthisis, it is evident 
that in the vast majority of human beings the lungs offer a good 
breeding-point for the tubercle bacilli. The localization of the bacilli 
is thus accomplished in the same manner as their localization in joints, 
the peritoneum, the meninges, ete.—by the blood stream. 

The hematogenous origin of phthisis is especially urged by Baum- 
garten, Ribbert, and Aufrecht. According to Baumgarten, tubercle 
bacilli in the inspired air may infect the mucous membranes of the 
upper respiratory tract whence they are carried by the lymphatics 
to the regional glands—the submaxillary, cervical, and supraclavicular, 
which are so often enlarged in tuberculous children. Entering the 
superior vena cava they may be carried by the blood stream to the 
lungs, causing typical interstitial tubercle of these organs and finally 
extend, while growing, to the alveolar walls, or within them. Aufrecht 
holds that the primary tuberculous lesion is always in the vascular 
walls, which are affected by bacilli brought to them by the blood 
stream. ‘Through the veins they pass into the right heart; or from 


54 TUBERCULOUS INFECTION 


tuberculous bronchial glands they get into the pulmonary artery or 
its branches, when the lymph channels are obliterated by inflamma- 
tory processes, into the finest bloodvessels and capillaries. Aufrecht 
has done quite some experimental work in support of his contention. 

It is thus clear that the aérogenous hypothesis of the origin of phthisis 
is explained by either a hematogenous or lymphogenous localization of the 
bacilli in the lungs. The frequency of tuberculosis of the glands, 
serous surfaces, and meninges speaks in favor of such origin of lung 
disease. The recent discoveries to the effect that a bacteremia is 
very frequent in phthisis support this contention. 

Infection by Ingestion.— The most important mode of hematogenous 
infection in phthisis should be the ingestion of tubercle bacilli, although 
it by no means excludes the air passages as portals of entry, because 
germs inhaled through the mouth, nose, and throat may be swallowed 
and pass into the blood through the mucous membranes at any point 
of the gastro-intestinal tract. However, in the vast majority of cases, 
it would be with food, especially with milk from tuberculous cows, 
that the bacilli would enter the body and cause disease. 

Simple as this theory appears, there are many objections to be 
considered before accepting it. The assertions of some authors that 
tubercle bacilli are invariably killed by the gastro-intestinal juices 
has been found largely incorrect, as was pointed out by Romer. To 
be sure, the gastro-intestinal juices may, and usually do, interfere 
with their rapid proliferation, and so may any fermentation in the 
intestinal tract, while the peristaltic movements of the intestines may 
soon remove them from the body; but they are not necessarily killed. 
Moreover, while a healthy, unbroken mucous membrane of the diges- 
tive tract is impermeable to tubercle bacilli, it is clear that a perfectly 
normal mucous membrane is very rare, considering the different kinds 
of food and its débris which pass through it, and the least disturbance 
in its anatomical structure or function may be sufficient to permit 
the passage of bacteria through its walls. 

Experimental investigations have shown that feeding guinea-pigs, 
rabbits, and monkeys with tuberculous sputum, or with pure cultures 
of tubercle bacilli, is effective in infecting the animal. Moreover, it 
has been found that the bacilli may pass through the intestinal walls 
into the blood or lymphatics without leaving any trace on the walls 
of the canal. 

Ravenel! conducted feeding experiments at the State Live Stock 
Sanitary Board of Pennsylvania and frequently observed extensive 
tuberculosis of the lungs and thoracic glands in animals which showed 
slight, or even no involvement of the intestine. He introduced into 
the stomach of a number of dogs tubercle bacilli suspended in an emul- 
sion of melted butter and warm water, using a tube in order to prevent 
possible infection through the trachea. The dogs were killed after 


1 Jour. Am. Med. Assn., 1916, 46, 613. 


INFECTION BY INGESTION 55 


three and one-half to four hours, during active digestion, as much 
chyle as possible was collected, and the mesenteric glands were removed. 
Guinea-pigs were inoculated with this material. Tubercle bacilli were 
demonstrated in 8 of 10 experiments. The dogs were kept on soft 
food for some days before the experiment, and were purged with castor 
oil, in order to rid the intestine of all foreign matter which might injure 
the mucous membrane. Numerous sections of the intestine were 
examined, but no injury could be detected. 

Because of this possibility of the tubercle bacilli entering the blood 
or lymph stream from the digestive tract, various authors have sug- 
gested the different parts of the canal, from the mouth to the rectum, 
as portals of entry of the bacilli, which are taken up by the blood and 
carried to the lungs where they finally stay and cause phthisis. Some 
have stated that irritated gums during dentition of infants offer a 
good portal of entry for the bacilli; the frequency of enlarged cervical 
glands at that period of life was cited as a good proof of the theory. 
Others have accused the tonsils, especially the pharyngeal tonsil. 
From the regional cervical glands some authors have traced the bacilli 
to the bronchial glands and finally to the lungs, though this has been 
shown by Wood! and Beitzke? not feasible for anatomical reasons. 
However, it must be acknowledged that even if there is no anatomical 
connection favoring the migration of bacilli from the cervical glands 
to the lungs, the microérganisms may be carried to any place by the 
blood. On the other hand, it must be mentioned that the tracheo- 
bronchial glands may be infected directly from the lungs by bacilli 
which have reached them with the inspired air. 

The most conclusive proof of the tubercle bacilli entering the lungs 
via the digestive tract has been brought forward by Calmette and his 
school, also by Whitla, and many others. Calmette* denies dust con- 
taining tubercle bacilli as a strong factor in phthisiogenesis. He could 
not produce anthracosis in animals after subjecting them to prolonged 
inhalation of air saturated with lamp-black. Introducing dry, or moist, 
tubercle bacilli directly into the trachea by inhalation or insufflation, 
or even by inoculation, they were never found to reach farther than 
the bifurcation of the trachea. Introducing lamp-black into the 
stomach through a tube, thus excluding inhalation, or mixing it with 
food, anthracosis was soon produced in the lungs of the animals. 
Similarly, tubercle bacilli introduced carefully into the stomach through 
a tube with a view of preventing aspiration into the trachea, invariably 
produced tuberculosis. 

Sir William Whitla’s! experiments along these lines are very instruc- 


1 Ann. Rep. Henry Phipps Inst., 1906, 4, 163. 

2 Virchow’s Archiv, 1906, 184, 1. 

3 Ann. de l’Inst. Pasteur, 1905, 19, 601; 1906, 20, 353. A more recent summary of 
Calmette’s work and views is found in his L’infection bacillaire et la tuberculose, Paris, 
1920, See especially pp. 145-156. 

4 Lancet, 1908, 2, 135. 


56 TUBERCULOUS INFECTION 


tive. He injected a mixture of China ink and water into the large 
vein in the ear of a rabbit. The animal was killed an hour later, 
and its lungs were found highly charged with carbon particles. He 
fed for four days a guinea-pig with an emulsion made by rubbing up 
finely powdered China ink in olive oil and water. The lung was found 
blackened by disseminated particles of carbon in the upper, and along 
the margins of the lower, lobes within from eight to twenty-four hours 
after a single dose. Whitla thus explains the migration of the carbon 
from the gastro-intestinal tract to the lungs: The carbon particles 
effect an easy entrance through the intestinal epithelial surface; reach- 
ing the lacteal or lymphatic paths they pass through the lymphatic 
glands of the mesentery, and finally, either inclosed in phagocytes or 
free, find their way into the thoracic duct to be poured into the venous 
circulation before being arrested in the capillaries of the lungs. Vas- 
steenburgh and Grysez’s experiments have also shown that it is easy 
to render an adult guinea-pig perfectly anthracotic without subjecting 
it to repeated inhalations of carbon particles. Considerable work along 
these lines has been done in this country. Schroeder and Cotton! 
found that no matter in what part of the body tubercle bacilli are 
inoculated, pulmonary disease may result. 

Calmette’s and Whitla’s experiments have been repeated by many 
other authors but their results did not confirm these investigators. 
Thus, Cobbett? fed animals with Indian or Chinese ink, or with soot, 
using very much larger quantities than Calmette and Whitla used, 
and not once only, but many times, and in some cases daily for one or 
more weeks. In some cases it appears that he found in the older 
animals some amount of pigmentation of the lungs. But he was careful 
to examine a large number of control animals (a precaution which 
seems to have been omitted by Calmette and the others) and he found 
just as much pigmentation in them as in those animals which had been 
fed with carbon. In young animals pigment was not seen, whether 
they had been fed with carbon or not. It was clear that some amount 
of pigmentation of lungs was to be reckoned with in the older, town- 
bred animals, and Cobbett remembered that he was accustomed to 
see a considerable amount of carbonization in the lungs of adult guinea- 
pigs when he was working in Sheffield. He therefore decided to repeat 
the experiments with country-bred animals; and when this was done 
no pulmonary pigmentation was seen in any of the animals, whether 
they had been made to swallow the ink or not. The anthracosis was 
thus not necessarily due to the carbon introduced experimentally. 

From these and many other experiments, contradictory though they 
are, we are safe in concluding that tuberculous infection, including 
phthisis, may be acquired through the ingestion of tubercle bacilli, and 
that the digestive tract permits the passage of the bacilli, which are carried 
by the blood and lymph streams to the various points of least resistance, 


1 Report of Bureau of Animal Industry, 1906, 23, 31. 
2 Jour. Pathol. and Bacter., 1910, 14, 563: The Causes of Tuberculosis, p. 146. 


MILK INFECTIONS 57 


of which, in the human being, the pulmonary apices appear to be the most 
vulnerable. 

It is, however, a question whether this mode of infection is the most 
common in spontaneous tuberculosis in humans. We must not over- 
look the fact, which has been established experimentally, that large 
numbers of bacilli are necessary to accomplish results; the normal gas- 
tro-intestinal tract can easily dispose of small doses of tubercle bacilli 
(see page 54.) 

Ingestion of tubercle bacilli may result in tuberculosis of the cervical 
or mesenteric glands, depending on the point at which the bacilli enter 
the upper or lower parts of the digestive canal. From these glands the 
bacilli are taken up by the circulating blood and carried to the tracheo- 
bronchial or mesenteric glands, and to the lungs. In many cases the 
bacilli remain dormant in these glands indefinitely, causing no disease 
at all; in others, the latency lasts only for some time, when finally, 
because of some exciting cause, they flare up again, migrate with the 
blood stream and, localizing in the lung, cause phthisis, and we then 
think that we are dealing with a new infection. 

Autopsies made by Gaffky,! Ungermann, Wollstein and Bartlett,’ 
Ghon,? Hamburger,‘ and others have shown that in children both 
glandular systems—the abdominal and the thoracic—are affected in 
nearly the same proportion. Primary infection of the intestine is very 
rare in adults, though in children it is quite common. Behring, how- 
ever, believes that all infections date back to early infancy when the 
bacilli are ingested, remain latent to flare up again in later years, 
causing disease of the lungs (see Chapter V). Of course, while making 
autopsies on adults who died from chronic tuberculosis it is difficult 
or impossible to find the point of primary inoculation. But in infants 
and children this may be done in many cases. Perhaps one of the best 
criteria is that in primary intestinal infection the mesenteric glands 
are implicated, while the intestinal mucous membrane may remain 
intact, and in secondary intestinal tuberculosis—the ulcerations so 
frequently found in phthisical subjects—the mesenteric glands are 
only rarely affected. Statistics of primary tuberculosis of the intestine 
in children are not in accord. From the data published by Orth, 
Eden, Councilman, Mallory and Pearce, Lubarsch, Wollstein and 
Bartlett, and many others, it appears that the percentage ranges from 
five to fifty. In children, a large proportion of these infections are due 
to bovine bacilli, as was already shown. 

Milk Infections.— The type of bacillus discovered in a case of tuber- 
culosis gives no positive clue as to the mode of its entry into the body. 
Of course, cow’s milk contains tubercle bacilli more often than has been 
generally appreciated; but they are not always of the bovine type. 
The studies of E. C. Schroeder,> John F. Anderson,® Ravenel, and _ 


1 Tuberkulosis, 1907, 6, 437. 2 Am. Jour. Child. Dis., 1914, 8, 362. 
8 Der primire Lungenherd bei der Tuberkulose der Kinder, Berlin, 1912. 

4 Die Tuberkulose des Kindesalter, Vienna, 1912. 

5 Bull. No. 99, Bureau of Animal Industry, Washington, 1907. 

6 Jour. Infect. Dis., 1908, 5, 107. 


58 TUBERCULOUS INFECTION 


others, have shown this to be a fact in this country. In New York 
City, Alfred F. Hess! found virulent tubercle bacilli in 16 per cent of 
107 specimens of milk retailed from cans. Inoculation experiments 
were carefully done and he found that guinea-pigs were infected with 
the milk, the cream, as well as the sediment. What is more noteworthy 
is that “commercially pasteurized” milk was also found to harbor 
tubercle bacilli. All bacilli were of the bovine type, with one excep- 
tion, in which the human variety was discovered. M. Rosenau? com- 
piled data concerning 551 samples of milk examined in which tubercle 
bacilli were found in 46, or 8.3 per cent, and he says that this may be 
taken as the average percentage for the entire country. 

It appears, hower er, that the dangers of milk infections have been 
overestimated by many writers. This is shown by two sets of facts. 
In countries in which the population does not use cow’s milk as a food 
at all, pulmonary tuberculosis is not at all lacking. This is the case 
in Japan, China, India, Egypt, ete., as has been shown by Kitasato.’ 
In the federated Malay states! tuberculosis has recently been increasing 
considerably, though bovine tuberculosis does not exist at all; among 
more than 250,000 pigs killed in the Ipoh abattoirs during four years 
no case of tuberculosis was found. In China cattle have been found 
free from tuberculosis. On the other hand, even if infection with bovine 
tubercle bacilli takes place, as it does very frequently, the potential 
dangers are slight, even in children. Thus, according to Kossel,® 
during the period 1905 to 1909 the Imperial Health Department in 
Germany investigated 113 cases of tuberculosis of the udder in cows. 
It was found that in only 44 cases their milk was being consumed after 
being boiled. Altogether 360 persons consumed the milk from these 
cows in a raw state (151 children, 200 adults, and 9 whose age was not 
ascertained). Itis noteworthy that they all, but 2, remained healthy. 
The 2 infected were infants, aged twenty-two and fifteen months. 
In both infants swelling of the cervical lymphatic glands occurred, 
and bacteriological examination, culturing, guinea-pig inoculation, and 
also cattle inoculation, revealed the presence of tubercle bacilli in these 
glands. But the general health of these infants remained good, no 
symptoms of any general disease appeared. ‘They were reéxamined 
one and a half, and two and a half years later and found thriving. 
In both these cases the tuberculous milk was consumed for relatively 
long periods of time, one year, and eighteen months respectively. 
No other cases of tuberculosis were observed in that family. Hess,° 
in New York City, followed for three years 18 children who drank 
milk in which tubercle bacilli were demonstrated and found that all 
but 1 remained free from tuberculous disease. Only in 1 had tuber- 
culous adenitis developed, and bacilli of the bovine type were culti- 
vated from the pus of the gland abscess. 

1 Jour. Am. Med. Assn., 1909, 52, 1011. 

2 Preventive Medicine, New York, 1913, p. 513. 

3 Sixth Intern. Congr. on Tuberculosis, 1908, 6, 1. 


4 Jour. Am. Med. Assn., 1921, 66, 785. 5 Deut. med. Wehnschr., 1910, 36, 349. 
6 Jour. Am. Med. Assn., 1911, 56, 1322. 


EXPERIMENTAL AND EPIDEMIOLOGICAL INFECTION 59 


Behring’s idea that most tuberculous disease in adults has been 
acquired during infancy by ingestion of milk derived from tuberculous 
cows is thus not entirely sustained. Statistics gathered by various 
investigators have shown that the disease is not more frequently found 
in adults who during infancy were hand-fed than in those who were 
breast-fed. 

Immunization by Bovine Tubercle Bacilli.— From the data arrayed 
in the preceding pages it appears that the tuberculous disease in chil- 
dren caused by bovine bacilli consists almost invariably in diseased 
glands, bones, joints, intestines, and skin, while fatal pulmonary infec- 
tions are extremely rare. There is ample evidence to the effect that 
the adult human is practically immune to the bovine type of tubercle 
bacilli, even if his immunity to the human type of bacilli has not yet 
been established to the satisfaction of all. Younger individuals, when 
infected with the bovine type of the bacilli, find it more or less easy 
to cope with the situation and recover, even though they finally emerge 
with disfigurement, and perhaps crippled. But if the problem of tuber- 
culosis was only that part which is produced by the bovine bacilli, 
it would not have by far the significance it has at present. In fact, 
several authors are of the opinion that these mild bovine infections 
immunize the organism against infections with the more virulent 
human type. In his investigations into the epidemiology of phthisis 
in Great Britain and Ireland, John Brownlee! arrives at the conclusion 
that “young adult” phthisis is less common in those counties from 
which a large amount of milk infected with tubercle is sent to the city 
of London. “ Drinking tuberculous milk probably infects many persons 
with tuberculosis of whom the great majority recover. The American 
physicians making postmortems in France on persons dying of wounds, 
found that 75 per cent had evidence of healed, or caseating, tubercle 
in the abdominal glands, though infection of the thoracic glands was 
comparatively rare. Apparently the only reasonable assumption to 
account for this relation is that some degree of immunity may be 
developed during childhood which persists into early adult ages. The 
larger the number of infants, therefore, exposed to infection in child- 
hood, the smaller the number found to take phthisis at the early adult 
age.” 

Distinction between Experimental and Epidemiological Infection. — 
From the data arrayed in this chapter it is clear that the enormous 
amount of experimental work done with the aim of shedding light on 
the problems of tuberculous infection has not entirely, or satisfactorily, 
explained the mode of entry of the bacilli into the human body. Of 
course, the contradictions in the experimental results obtained by 
various investigators may be explained easily by the various methods 
pursued in investigations, the different cultures and infecting doses 
employed, the character of the culture media, the species of animals 
used, ete. But after discounting all these variable factors, it remains 


1 An Investigation into the Epidemiology of Phthisis in Great Britain and Ireland, 
Medical Research Committee, Special Report Series, London, 1920, No. 46, p. 54. 


60 TUBERCULOUS INFECTION 


a fact that hardly any of the experimental modes of infection have com- 
pletely imitated natural conditions as observed among human beings. 

It is therefore important to emphasize the immense distinction 
between experimental and epidemiological infection and immunity 
when considering tuberculosis in human beings. We know of many 
diseases which only rarely, or never, occur spontaneously in certain 
animals, but which may be induced experimentally. This is perhaps 
best seen in guinea-pigs which only rarely acquire tuberculosis under 
natural conditions, while experimentally they are found to be exceed- 
ingly susceptible, thus indicating that because we may induce a certain 
disease experimentally, this is not necessarily the manner in which the 
disease is engendered under natural conditions. It also shows that 
while we may infect a guinea-pig in a certain manner, it does not follow 
that humans are, under natural conditions, infected in the same manner. 

We have seen that experimental infection does not produce the 
same results in different animals even when induced in the same 
identical manner, and with the same culture and dose of bacteria. 
When guinea-pigs are inoculated subcutaneously with bovine bacilli, 
the spleen is first affected, then the liver, while the kidneys are almost 
invariably spared; in the rabbit, next to the lungs, the kidneys are 
affected. The lung of the hen is practically refractory to the typus 
gallinaceus of the acid-fast bacilli. After inoculation of bovine bacilli 
the lymph glands are nearly always affected in the rabbit, but they are 
spared when human bacilli are used. Inasmuch as the visceral organs 
are affected after the virus is introduced through the subcutaneous 
route, it is evident that the bacilli pass through the regional lymphatics 
without producing visible harm. Comparative pathology abounds in 
examples which indicate that the various strains of the bacilli have 
different effects not only on different animals, but also on the same 
animal under different conditions. And when we bear in mind that 
the most common type of tuberculous disease, chronic phthisis, is 
distinctly a human disease which never occurs in animals sponta- 
neously, and which has never been induced experimentally, it is ap- 
parent why experimental infection has not cleared up the problems of 
phthisiogenesis. 

We have seen that there is no agreement between authorities as to 
the most common channel of entry of the tubercle bacilli; and Rémer, 
perhaps the most indefatigable worker in the field of tuberculosis, 
arrived at the conclusion that there is evidently some mode of transmis- 
sion of this disease with which we are as yet unacquainted. 

It must, however, be mentioned here, a point which will be dis- 
cussed in detail later on, that in human beings infection alone is not 
sufficient to produce disease; after all, disease occurs only in a com- 
paratively small proportion of persons infected with tubercle bacilli. 
In other words, while there is no tuberculosis without tubercle bacilli, 
these microérganisms harm only those who are predisposed to the 
disease. We are more and more becoming convinced that phthisio- 
genesis is more a problem of predisposition than of bacterial infection. 


CHAPTER ITI. 
THE EPIDEMIOLOGY OF TUBERCULOSIS. 


Ubiquity of the Tubercle Bacillus.—In our survey of the biological 
characteristics and the channels of entry of the tubercle bacilli we found 
that the virus of tuberculosis is ubiquitous; that it is found wherever 
civilized human beings congregate, because tuberculous human beings 
expectorate sputum containing these bacilli, and domestic animals 
affected with this disease are everywhere. It has been estimated that 
the number of bacilli discharged daily in the sputum of a single patient 
with advanced phthisis is as great as the number of human beings on 
the earth. The modest estimate mentioned by Cornet may be taken 
as near the truth—that 7,200,000,000 bacilli may be thrown off daily 
from a single patient. If we imagine each organism placed end to end 
in a single file, this number would constitute a chain not less than 
twelve miles in length. 

Clinical and experimental medicine have shown conclusively that 
the expectoration of consumptives, milk from tuberculous animals, 
etc., are capable of causing infection; that these microdrganisms may 
enter the body through wounds, as well as through the unbroken 
skin, and the mucous surfaces of the respiratory and alimentary tracts, 
etc. We have also shown that though there are many hindrances 

-in the way of infection, still, when everything stated in the preceding 
chapter is considered, it is not surprising that one out of eight in 
civilized countries succumbs to the disease, but that the other seven 
escape its ravages. 

Tuberculous Infection vs. Tuberculous Disease.— As a matter of 
fact very few escape infection with the tubercle bacilli, especially 
those living in large industrial cities. Making this statement it must 
be emphasized that a distinction is to be made between tuberculous 
infection and tuberculous disease. ‘The latter refers to the disease 
known for centuries, ever since Hippocrates described it, as consump- 
tion, or the equivalent of the term found in all European languages. 
It is the disease which causes more than 95 per cent of the suffering, 
social and economic misery and deaths due to the tubercle bacilli. 
On the other hand, tuberculous infection covers all the cases in which 
the virus of tuberculosis has entered the body, irrespective of whether 
it has caused clinically appreciable disease, or not. Tuberculous disease 
is always preceded by infection, but infection with the tubercle bacilli is 
not invariably followed by disease. 

Research of the past three decades has shown conclusively that 


62 THE EPIDEMIOLOGY OF TUBERCULOSIS 


infection with tubercle bacilli is not invariably followed by that train 
of symptoms which we observe in phthisis; that it does not necessarily 
cause sickness, excepting an altered reactivity to tuberculin. Appar- 
ently more people harbor the bacilli within their bodies, or show 
traces of having harbored them, without knowing it at all, than such 
as suffer, or succumb, as a result of tuberculosis of the lungs, or of 
other organs. These persons are undoubtedly tuberculous, and there 
are many strong reasons for the assumption that, like other bacillus 
“carriers,” they are liable to cause mild infections in others. But they 
are not at all phthisical in the clinical sense. Some of them are destined 
to become phthisical; in fact, practically all phthisis evolves from an 
infection acquired during childhood, as we shall show when discussing 
phthisiogenesis. 

Frequency of Tuberculous Infection.—Careful and painstaking 
scientific investigations have shown that the frequency of tuberculous 
infection goes hand-in-hand with civilization, or contact of primitive 
peoples with civilized humanity. In modern large cities very few 
persons escape infection. Autopsies made with a view of ascertaining 
traces of tuberculous lesions, both active and healed, have shown that 
over 90 per cent of adults are thus affected among the civilized; but 
among primitive peoples, who have not come in contact with civilized con- 
ditions and humanity, no tuberculous changes are found at autopsies. 

In Laennec’s! classical work on diseases of the lungs published in 
1831 we find the following in a footnote: “M. Lombard’s investiga- 
tions in the Children’s Hospital at Paris show that of the children who 
die between one and two years of age, one-eighth are tuberculous; 
between two and three, two-sevenths; between three and four, four- 
sevenths; between four and five, three-fourths. In the succeeding 
years up to puberty, tubercles are found more frequently than before 
the fourth, but much less frequently than from the fourth to the 
fifth. Papavoine, of the same hospital, found that the number of 
tuberculous children between the fourth and eleventh years is greater 
than those who are not tuberculous, tubercles being particularly 
prevalent from the fourth to the seventh years. Their frequency is 
again increased about the twelfth and thirteenth years, and at four- 
teen and fifteen years the rate of prevalence is the same as at four 
and five. These results were obtained from investigations made on 
910 children (888 boys and 522 girls); somewhat less than three-fifths 
were tuberculous.” 

Similarly, Henry Ancell? emphasized the extent of tuberculous disease 
in London as far back as 1840. In a paper on “Facts and Opinions 
Relating to Tuberculosis, with Commentaries,” he cites the Decennium 
Pathologicum of Dr. L. IX. Chambers, giving the results of the post- 
mortem examinations made in the mortuary of St. George’s Hospital 


1 Traité de auscultation médiate et des maladies des poumons et du cceur, Paris, 
1831, 2, 125. 
2 Assn. Med. Jour., 1853, p. 1030; quoted from Karl Pearson, loc. cit., p. 19, 


FREQUENCY OF TUBERCULOUS INFECTION 63 


in the ten years, December 31, 1840, to December 31, 1850. The 
number of autopsies was 2046. The following are the figures: 


Birth to ; Above 

15 years. 15 to 30. 30 to 45. 45 to 60. 60. All, 
Total number of autopsies . . . 154 636 651 438 167 2046 
Per cent of tubercle found . . . 29.7 a iats) 25.8 19.6 That 26.1 


It appears that these facts were entirely forgotten, and medical 
literature was silent about the extent of tuberculous infection, and 
changes in the bodies of many who have shown no indication of this 
specific disease during life, until in 1900 Naegeli! published his report of 
500 autopsies at the Pathological Institute at Zurich. He found 71 
per cent showed pathological changes due to tuberculosis. Among 
individuals under eighteen years of age, only 25 per cent showed such 
lesions, mostly of a grave character, often leading to a fatal termina- 
tion. But in persons above eighteen years of age the proportion that 
showed traces of tuberculous infection reached 98 per cent. Of these, 
only 28 per cent died as a result of this disease, while the rest had 
tuberculous foci which were either altogether healed, or quiescent, or 
slowly progressing. 

When first published this revelation appeared incredible, but then 
other pathologists investigated autopsy material along the same lines, 
and they practically confirmed Naegeli’s findings. From the work 
of Harbitz, Scheel, Burckhardt, Lubarsch, Adami and McCrae,? and 
many others, it is clear that very few persons escape infection with 
tubercle bacilli before reaching the age of maturity. They have all 
found that no matter what the. cause of death may have been, whether 
the persons knew that they had been tuberculous or not, between 50 and 
100 per cent of people hving in large cities show active, quiescent or 
healed tuberculous lesions in some organs of their bodies. On this point 
all are now in agreement, the only dispute which may be found in the 
literature consists in whether the percentage is only 70, or reaches as 
high as 100. Thus, Lubarsch® states that Naegeli exaggerated his 
findings, because of 7371 necropsies performed by Naegeli, Burck- 
hardt, Risel and Lubarsch, only 4230, or 57.4 per cent, showed tuber- 
culous changes; of 5796 necropsies on adults, 4017, or 69.2 per cent, 
showed such changes. 

These autopsies showed another significant fact: The newborn 
infant is invariably free from tuberculosis, indicating that infection, 
uf vt occurs at all, always takes place after birth. Among infants dying 
during the first year of life from any cause, some are found presenting 
lesions of a tuberculous character, while beginning with the second 
year the number of infected children increases steadily, so that at the 
age of fifteen there are nearly as many tuberculous among them as 
among adults. In this country Martha Wollstein and F. H. Bartlett‘ 
reported 1320 autopsies performed at the Babies’ Hospital in New York 

Virchow’s Arch., 1900, 160, 426. 
2 Tr. Sixth Internat. Congr. on Tuberculosis, 1908, 1, 325, 


vt 

2 

3 Virchow’s Arch., 1913, 213, 417. 

4 Am. Jour. Dis. Children, 1914, 8, 364. 


64 THE EPIDEMIOLOGY OF TUBERCULOSIS 


City on children under five years of age, of which 118, or 13.5 per cent, 
showed tuberculous changes. In Europe the proportion is even higher, 
as is evident: from the findings of Naegeli, Burckhardt, Lubarsch, 
Hamburger, and many others. 

In England autopsy material has shown the same conditions. East- 
wood and F. Griffith, in London, and A. S. Griffith, in Cambridge,! 
have examined the organs and glands of 215 children who died from 
various causes in general hospitals, inoculating animals, ete. The pro- 
portion harboring tubercle bacilli is shown in the following table: 


Number infected with Proportion 
Age. tubercle bacilli. infected. 
O t6° -2iyears ean. Be ee eee 6 out of 17 35 per cent 
2 toi a Sie ide Se, EY ee LS ie pny 52 % 
440) 6.7 = Leet Ween eee OO 2 sy 58 ~ 
oto LORS: o SP ieee kee Os, Be59 Sonera rize ¢ 
LO toe 2 aes So tte See alee 2 vs 3 


{ven conceding that among children who succumb the number of 
tuberculous is likely to be higher than among those who survive, the 
proportion is still very high—60 per cent of all children are shown 
to have been infected with tubercle. 

Another series of autopsies on children has been reported by Har- 
bitz.2. In the Anatomical Institute at Christiania, Sweden, during 
1898 to 1911, the bodies of 484 children who died from any cause 
were dissected. The ages ranged from birth to fifteen years. His 
results are given in the following figures: 


Number Tuberculous lesions: 
Age. examined, Per cent. 
Octo. year G3 Gis eo ee ae ei ee se ee, eee 20.0 
1 tO. 22 Years' Sn are eee orn ee ge 65 26.2 
Ssbor tes es Sa ee ee 44 31.8 
5to. 6 > cnet he. ee ee Se 28 67.9 
760. 10. oo iil ey Bin nein CSL Re Oe Ri 53 62.2 
DL tO TA Se ee ee en ee ees eee ee 53 Sil 
15: SF OR CAG ae Opt eee eee 40 80.0 
Total... Adina S) Skee, Si ies been ok ee med 41.08 


The anatomical picture was predominantly that of tuberculosis of 
the lungs and the lymphatic glands, especially those of the thorax. 
The younger the child, the more acute and progressive the lesion 
found. In only 1 case could he suspect congenital tuberculosis. 

The most recent series of autopsies reported are those collected by 
A. Reinhart.’ For eighteen months he made a special study of all cases 
that came to autopsy at the Berne Pathological Institute, looking for 
evidences as to the frequency of tuberculous lesions. In all he per- 
formed 460 autopsies. Among the 28 newborn infants no traces of 
tuberculosis were found; in 72 children under sixteen years of age, 
29.16 per cent showed active tuberculous lesions, although only 16.8 
per cent had succumbed to this disease. He again confirmed the results 


1 Report to the Local Government Board on Public Health, N.8., No. 88, 
2 Norsk mag. f. Laegevidesk., 1913, 5 R., 11, 1. 
3 Cor.-Bl., f. schweiz. Aerzte, 1917, 47, 1153. 


FREQUENCY OF TUBERCULOUS INFECTION 65 


of nearly all other pathologists to the effect that the number of tuber- 
culous lesions increases with the advance of the age of the children. 
The infants under one year suffered the least, only 7.14 per cent. 
Among 360 cadavers of adults, 96.38 per cent were found with tuber- 
culous lesions; negative results were encountered in only 13 cadavers, 
and of these 9 were under thirty years of age. Here again there is 
evidence that most tuberculous lesions heal: In 63.9 per cent of the 
adults the lesions were found healed; the older the individuals, the 
higher the proportion of healed lesions. It is also noteworthy that the 
difference between the incidence of healed lesions in town dwellers 
(92.9 per cent) and country dwellers (98.1 per cent) is rather slight. 

Another point has been brought out by these autopsies which is of 
immense epidemiological and clinical importance. The tuberculous 
lesions found at the autopsies are not all active, nor were they the cause 
of death in many cases. Indeed, there were many which were latent, 
quiescent, or even healed. Thus among the 406 tuberculous bodies 
examined by Naegeli, 28.1 per cent had healed or latent lesions; among 
Burckhardt’s 1452 autopsies he found 1221, or 84.1 per cent, tubercu- 
lous; but 39.4 per cent of them showed quiescent latent, or healed 
lesions, and Reinhart found 70 per cent inactive lesions. The results 
of nearly all other investigations show the same conditions. 

Active and progressive lesions, leading to death, are characteristic 
of infancy; in fact, during the first vear of life all lesions discovered 
at autopsies are those of generalized and progressive tuberculosis. 
Localized lesions are rare in childhood; they only make their appearance 
after the second year, and are still rare at ten years of age. Available 
pathological evidence tends to show that the younger the individual 
infected with tuberculosis, the more likely he vs to be killed by the disease, 
while the older the indwidual, the less rs he likely to suffer from acute and 
progressive disease. In fact, Lubarsch says that among older persons 
tuberculosis is a relatively harmless process, showing, as it does, a 
strong tendency to latency or healing. He illustrates this point by the 
following statistical facts: 

Among 502 infants under one year examined after death, 4.58 per 
cent were found with tuberculous lesions, all of which were acute or 
subacute general tuberculosis, without any tendency to localization 
in a single organ. Of 123 children two years of age, 20.3 per cent 
were found with tuberculous lesions. All were also active and pro- 
gressive, though there were already seen tendencies to localization of 
the process, but no calcification was noted. At three years of age 
24.7 per cent of the bodies showed tuberculous changes, and in one 
some evidences of calcification were found microscopically in a tuber- 
culous bronchial gland. He found that the number of active and 
fatal cases of tuberculosis keeps up at a high level until the age of fifteen, 
when localized tuberculosis begins to manifest itself, though the 
lesions still show tendencies to progression, and calcification is still 
exceptional. Thus, among 139 bodies of tuberculous individuals 
between one and sixteen years of age, only 33, or 23.7 per cent, showed 


5 


66 THE EPIDEMIOLOGY OF TUBERCULOSIS 


calcified foci, but none was completely healed—all were active and 
progressive in character. 

Only after the seventeenth year of life are to be noted at autopsies 
latent and healed tuberculous lesions, and they keep on increasing 
in frequency, so that at the age of forty they are more frequent than 
progressive lesions. The following table, as well as Fig. 3, shows the 
point clearly: 


Latent and 
Active lesions. healed lesions. 

Age. Per cent. Per cent. 
LE.00 . DOs es dee re eo el eet eh re ee A, 22.6 
20 tO" 30-2 % wget ee ey ne Bea ee ns ee Oy 7) 23.9 
30'to’ 40%) Gea Nees ae eee ee eee GO 47.4 
40 to -5O: <w acy, G4 -aye Arey, Sacer Lee So) Gist 
50 to: GO x. > aehs ee, oe ei ee ee Me 66.5 
60 to TO oe Pee ce ice a ee an eee ch cy (Aor ve 
70:40) 2802 SE eee a a ee ee) a7 85.3 
S80. t0,2.90 4.5: Sine hth ee re ee een Domne 9.3 90.7 
90'to: LOO ic. Vat ne eae cn Le ee 0.0 100.0 


These data must be considered underestimates, rather than over- 
estimates, because while dissecting lungs and pleure slight and healed 
lesions may be overlooked, unless serial sections are made. Eugene L. 
Opie,! of St. Louis, attempted to overcome this possible source of error 
by an ingenious method. While making autopsies on 93 children, 
under eighteen years of age, and 50 adults, he roentgenographed each 
lung, and since calcium salts are impervious to the roentgen rays, 
small nodules which could not be detected on inspection and dissec- 
tion were easily discovered. He thus found that partially calcified 
foci containing caseous material of soft, friable consistence are con- 
spicuous in roentgen-ray plates. In some specimens tuberculous 
nodules seen on the plate could not easily be found on dissection, 
but careful search always revealed them. In all doubtful cases con- 
cerning the nature of a lesion, microscopic examination of the tissue 
was made. It is thus clear that Opie’s work was very carefully done. 

His results are given in the following table: 











Tuberculosis. 
In those who 
Age (years). | Number of Present. aici 
Fatal. Non-fatal diseases. 
Number. | Per cent. 
| 

Winders ales me Nie 43 4 9.3 4 0 0.0 
1 GOs ta Shee eae 16 1 622 1 0 0.0 
DLO pe Oe Saee ae 14 6 42.8 3 3 PAs) 
DebORiOy te acme 11 5 45.5 2 3 Soc 
AMO MOSES oe Oe een 9 6 66.7 1 5 62.5 
1S to. Ore eae eee 6 6 100.0 1 5 100.0 
SOONG! we eee me 23 23 100.0 1 22 100.0 
50! 007 Oe eee ee 15 15 100.0 1 14 100.0 
7O and over. . . 6 6 100.0 0 6 100.0 























1 Jour. Exper. Med., 1917, 25, 885; 26, 263. 


67 


FREQUENCY OF TUBERCULOUS INFECTION 


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6S THE EPIDEMIOLOGY OF TUBERCULOSIS 


Here again it is clear that in this country the number of persons 
infected with tuberculosis is not less than has been observed in Europe, 
though most of the lesions have not been the cause of death, but have 
healed, leaving but scars, or calcified nodules. “The age of incidence 
of focal tuberculous lesions of the lungs,’’ says Opie, “demonstrates 
that they have their origin in most instances in childhood. Focal 
lesions which heal have been found at all ages after the second year of 
life, but in more than half of all individuals these lesions are acquired 
between the ages of ten and eighteen years. In the period between 
eighteen and thirty at least 85 per cent of all individuals have acquired 
focal tuberculous lesions. The occurrence of tuberculous infection in 
the lungs, in the regional lymphatic nodes, or in some other organs of 
the body, such as the gastro-intestinal tract and its lymphatic system, 
is nearly universal, but doubtless a few individuals escape. That focal 
tuberculous lesions of the lung are occasionally acquired during adult 
life is shown by the slight increase in the proportion of those with 
these lesions as age increases from eighteen years to old age.”’ 

The frightful tuberculization of humanity, as revealed by these 
autopsy findings, was explained by some authors as due to the fact 
that in hospitals there is a concentration of tuberculous sick, and among 
children who succumb at an early age, the percentage of tuberculous 
should be much higher than among those who survive until maturity. 
But it must be recalled that these autopsy findings were obtained in 
children who died from all causes, and that in many the tuberculous 
lesions were found incidentally, although the causes of death were 
entirely different diseases. 

Reliability of Autopsy Statistics.— Many objections have been raised 
against these autopsy statistics showing that nearly every adult living 
in a modern city harbors tubercle bacilli within the body. Some 
have maintained that many non-tuberculous changes in the lungs 
and pleura have been included as “latent” or “healed” tuberculosis. 
But Naegeli, Burckhardt, Reinhart, Opie, Griffith, and many others, 
state distinctly that extreme care had been taken before pronouncing 
doubtful pathological changes as tuberculous. Some, like Opie and 
Reinhart, have made microscopical studies of the tissues before decid- 
ing; Griffith inoculated guinea-pigs, ete., before deciding. 

It has also been suggested, especially by Cornet, that these latent 
lesions were caused by avirulent, or mildly virulent tubercle bacilli, 
perhaps even by some of the non-pathogenic acid-fast microdrganisms 
which abound in nature. But this has been disproved for the first 
time by Loomis, who injected such glands into rabbits and found 
that they were infected with tuberculosis. Cobbett,! working for the 
Royal Commission on Tuberculosis in England, found that definitely 
caseous nodules taken from the lymphatic glands of children might 
be quite incapable of setting up tuberculosis when emulsified and 


1 The Causes of Tuberculosis, p, 70, 


RELIABILITY OF AUTOPSY STATISTICS 69 


injected into animals, even when the injections were made in such a 
susceptible animal as the guinea-pig. This was surprising, but what 
was more surprising still, the caseous matter thus shown to be totally 
devoid of infective power might contain plenty of well-formed tubercle 
bacilli, easily visible under the microscope. Similar experiences were 
recorded by A. S. Griffith, Weber, and others. This would tend to con- 
firm Cornet’s view that the lesions were produced by avirulent, or 
mildly virulent, tubercle bacilli, and for this reason the disease they 
produced was not active, nor fatal. But other investigators did find 
virulent tubercle bacilli. Thus, Lydia Rabinowitsch! found that com- 
pletely calcified glands, in which no tubercle bacilli could be discovered 
microscopically, were still capable of infecting animals. Eastwood and 
Griffith even cultivated tubercle bacilli from glands of 72 children, 
34 of whom were apparently non-tuberculous. 

It is thus clear that the tubercle bacilli found in the healed lesions 
of persons who have succumbed to diseases other than tuberculosis are 
often alive and virulent. 

The objection has also been raised that the autopsy material 
obtained in morgues in large cities represents the lowest grades of 
society, the poorest strata of population, who are most likely to suc- 
cumb to tuberculosis, while the well-to-do, or self-supporting elements 
of society, even in cities, are by no means tuberculous to such an 
appalling extent. But it is the poor who present the problem of tuber- 
culosis most acutely. Moreover, Naegeli pointed out that his material 
was not exclusively of the lowest strata of society. Forty per cent at 
least were country folk, and 6.5 per cent were private patients; only 
in 22.5 per cent was tuberculosis the cause of death, as against 28 per 
cent occurring among the general population of the Canton of Zurich, 
thus showing that the persons on whom he made his autopsies were not 
excessively tuberculized. 

Better confirmation of these findings was, however, supplied by 
several series of autopsies made on persons who had enjoyed good 
health but succumbed to accidents, or acute diseases. Among 826 
autopsies made on such individuals, Birch-Hirschfeld? found 171, 
or 20.7 per cent, with tuberculous lesions. Of these, 105, or 12.7 
per cent, were healed lesions; 31, or 3.8 per cent, were actively ad- 
vanced; 35, or 4.2 per cent, were latent or mildly active. Similar 
results were reported by J. G. Monckenberg,’ who made autopsies on 
85 soldiers fallen in the World War. In 25, or 31.76 per cent, he 
found distinct evidences of active, latent, or healed tuberculosis. In 
5 cases the lesions were so active that they may have been the cause 
of death, but in the remaining 22 cases the tuberculous lesions were 
incidental findings. Likewise, Hart* made autopsies on 573 soldiers 


1 Berl. klin. Wehnschr., 1907, p. 35. 

2 Deutsch. Arch. f. klin. Med., 1899, 64, 58. 
3 Ztschr. f. Tuberk., 1915, 24, 33. 

4 Tbid., 1919, 31, 129. 


70 THE EPIDEMIOLOGY OF TUBERCULOSIS 


who died from non-tuberculous diseases during the war, and found 
that 196, or 34 per cent, had tuberculous lesions, of which 151, or 26.8 
per cent, were “obsolete.” 

Extent of Tuberculous Infection among the Living.— The extent of 
tuberculous infection among the living population has been ascertained 
by the application of the tuberculin test, which is even more delicate 
than the macroscopic examination of the body after death, showing, 
as it does, the number of persons infected with tubercle bacilli and 
who have survived, or have not at all suffered as a result of the infec- 
tion. No matter how slight the lesion produced by the tubercle bacilli, 
the tuberculin test reveals it. 

Extensive investigations have been made along these lines, and it 
was found that there are very few adults living in cities who do not 
react to tuberculin. Those who live in tubercle-laden surroundings 
hardly ever escape infection. Pollak! found that in Vienna 96 per 
cent of children of tuberculous parentage were infected before they 
reached the fourth year of life. In Spain, Munoyerro and Frias? 
found tuberculosis in 195 of 3000 children from one to three years of 
age at a Madrid asylum. The tuberculin tests showed 6.3 per cent 
of infections at this early age, and the tuberculous cadavers formed 
9.3 per cent of the total. In Argentina, Garrahan’ applied the tuber- 
culin test, often three or four times, to 1214 children at Buenos Aires, 
between two and sixteen years of age. He found that of the children 
between fourteen and sixteen, 75 per cent showed signs of tuberculous 
infection. Mantoux‘! found that 84 per cent of the children in Paris 
were infected before they reached the fifteenth year. A more recent 
investigation by Germaine Mioche,® who applied the tuberculin test 
to 2784 children at Paris, gave the following proportion of positive 


reactions: 
Age. Number of cases. Per cent positive. 
Under 3.01 ths geist ee ce 298 aah, 
3) to; 6months * tees foe te le nealace es. ee ruee one 459 (fer? 
6tto 2 months) eee oe cs eee ee ee 583 16.8 
Winder ‘ly years.) Gee Oe hon eee a mh) 10.6 
[to 2" years.) eee te nog oie eek ee eee ae 247 24.3 
2: t0> +) years: (ae 221 ete bale) gee ice ee ae Fae 467 56.8 
§:to 10years..20 P¥ ee Tee eee 525 67.4 
LOGO tLDNYy ears 0 see nee Ps a ee Se he 302 82.7 


In New York City the author® has found that children living with 
their tuberculous parents are infected to the extent of 84 per cent at 
the age of fourteen, as can be seen from the table and the attached 
diagram (Fig. 4). Similar results have been obtained while testing 
large numbers of children of tuberculous parentage in various European 
cities. 

1 Brauer’s Beitr., 1911, 19, 469. 

2 Arch. Espanoles de Pediatria, 1919, 3, 532. 

3 Semana Medica, 1919, 26, 771. 

4 Sémaine méd., 1909, 29, 371; Presse méd., 1910, 18, 10. 
5 Le Nourisson, 1920, 8, 41. 

6 Arch, Pediat., 1914, 31, 96, 197. 


TUBERCULOUS INFECTION AMONG THE LIVING ral 


Taking apparently healthy children at random, 7. e., those who 
do not live in homes harboring evidently tuberculous persons, it 
appears that they are also infected in large numbers. Hamburger! 
found that at the age of fourteen 94 per cent of the children of artisans 
in Vienna show signs of infection with tuberculosis. Calmette? at 


TABLE SHOWING EXTENT OF TUBERCULOUS INFECTION AMONG THE POORER CLASSES 
IN New York City BASED ON THE APPLICATION OF THE TUBERCULIN 
Test on 1280 CHILDREN UNDER FIFTEEN YEARS OF AGE. 


Percentage giving positive reactions among 









































































































































































































= Children of tuberculous Children of non-tuberculous 
parents. parents. 
Number of Number of 
Age. cases. Per cent. cases. Per cent. 
Under lyedregss -5 «a 7) 35 J15.15 56 10.07 
ETOURA TV CATS a. =r oetat, 84 49 55.10 39 Siar 
SEO we 80 ote el eee 90 68.88 SO 41.25 
yates, ee ear wore See 95 65.26 106 50.00 
Con meee nD ee ae oe ee ae (Aleaal 173 64.74 
Stop la ea pele ae ee ae 18 1 74.58 134 69.40 
14° ee eee cat Sif 83.79 20 75.00 
100 
90 
80 
70 
‘at 
Z 60 i 
Ww 
O fia 
ie pain 
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ssi 








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i= 


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SecaH eect | 
scat 


AGE 6nos. 6-12mo0s.2yrs. 3 4 5 





7 8 
YEARS 


Fig. 4.—Proportion of children reacting to the cutaneous tuberculin test. Black 
line represents 692 children of tuberculous parentage in New York City; dotted line 
represents 588 children of non-tuberculous parentage in New York City. 


Lille, France, testing 1226 persons of all ages taken at random from 
diverse social strata, all apparently healthy, found that during the 
first year of life only 9 per cent were infected, but the percentage 
kept on increasing, so that at the age of fifteen and over, 87 per cent 


1 Die Tuberkulose im Kindesalter, Berlin, 1913. 
2 Grysez et Letulle, Presse méd., 1911, 19, 651. 


72 THE EPIDEMIOLOGY OF TUBERCULOSIS 


were infected. In New York City the author! found while testing 
children of poor, but non-tuberculous parentage, that under one year 
of age 10 per cent were infected; between one and two years of age, 
33.33 per cent, and the proportion giving positive reactions to tuber- 
culin kept on growing steadily with advancing age, so that at the age 
of fourteen, 75 per cent of “reactors” were found. 

It is well known that the von Pirquet test, which was used in these 
cases, is occasionally negative when applied the first time, but is 
positive when applied a second or third time. For this reason some 
who have applied the test but once found a lesser number of reactors. 
J. B. Manning and H. J. Knott,’ in Seattle, tested 228 children, aged 
ten to fourteen years, coming to the Children’s Tuberculosis Clinic, 
the large majority of whom were from tuberculous homes. Of 166 
with a definite history of exposure, 84, or 50.6 per cent, gave a positive 
von Pirquet test, though 82.1 per cent of these children showed no 
clinical evidences of tuberculosis. Of 62 children with no history of 
exposure, 14, or 22.8 per cent, were reactors. But they used only one- 
half strength of tuberculin, and when found negative after the first 
application the test was not repeated. Had they applied it twice or 
three times, and in full strength, the proportion of reactors would 
undoubtedly have been higher. George H. Cattermole’ tested children 
in Boulder, Colorado, where there is no overcrowding, but plenty of 
good food and sunshine. Probably one-half the families in Colorado 
contain one or more adult consumptives. It would be expected that 
the number of reactors should be quite large. Yet only 38 per cent 
were found to have been infected. This anomaly may be explained 
by the superior social and economic conditions, but it seems to me 
that the following reasons are more plausible: The number of children 
was rather small, only 66; if he had extended his investigations the 
results might have been different; he applied the test but once in 
most cases, using the von Pirquet and the Moro tests. At any rate 
it appears that opportunities for infection were not altogether counter- 
balanced by superior climatic and economic conditions. 

While it is in large industrial cities that tuberculosis is most wide- 
spread, as is shown by the high morbidity and mortality from the 
disease, infection is not lacking in rural communities of civilized 
countries. Investigations made by Jacob,‘ Hillenberg,’ Overland,® and 
others have shown that in villages, where a case of open tuberculosis 
had not been seen for many years, the people living under good 
economic and hygienic surroundings, and where the milk supply was 
practically free from tuberculous contamination, 25 per cent of the 


1 Arch. Pediat., 1915, 32, 20. 

2 Am. Jour. Dis. of Children, 1915, 10, 354. 

3 Jour. Am. Med. Assn., 1915, 65, 782. 

4 Die Tuberkulose und die hygienische Misstiinde auf dem Lande, Berlin, 1911. 
5 Tuberkulosis, 1911, 10, 254. 

® Internat. Zentralbl. f. Tuberkulose, 1914, 8, 635. 


SUSCEPTIBILITY TO TUBERCULOUS INFECTION ie 


school children and about 45 per cent of the adults gave positive 
reactions to tuberculin, indicating that they had not escaped tuber- 
culous infection. Here we find that the effect of infection is only an 
altered reactivity to tuberculin, and not phthisis. The reasons for 
this phenomenon will be discussed later on. 

Tuberculosis among Primitive Peoples and Races.— The only regions 
free from tuberculosis appear to be those inhabited by primitive peoples 
who have not come in contact with civilization. Thus, the American 
Indian, before the advent of the white man on this continent, knew 
nothing of the disease, as was shown by Woods Hutchinson,! Hrdlicka,? 
and others. Nor do the savage and barbarian races of Central Africa 
and Asia seem to have had experience with tuberculosis, until the 
whites brought it to them. Among these primitive peoples the tuber- 
culin reaction is always negative, and autopsies made on their dead 
reveal no active or healed tuberculous lesions, as is the case with new- 
born infants among Europeans. But it appears that as soon as these 
peoples come into contact with civilized man they are infected in large 
numbers. This was observed among the American Indians, the native 
tribes of Australia and Africa, ete. The application of the tuberculin 
test among these races by Calmette,*? Metchnikoff,! Ziemann,’ and others 
has shown clearly that the frequency of tuberculous infection depends 
directly on their contact with civilization. It is altogether absent, 
or extremely rare, among those races who have recently met the 
white man, but the proportion grows in direct ratio to the intensity 
of immigration of European settlers, and with commercial interchange 
between them and civilized humanity. It is also evident that their 
immunity from this disease before the advent of the white man was 
not due to racial or climatic conditions, as was suggested by some earlier 
writers, but solely to the absence of tubercle bacilli, because as soon 
as these are imported, the natives display a striking vulnerability to 
the disease, which is greater the longer they have been protected 
against the importation of tubercle bacilli. 

Racial Differences in Susceptibility to Tuberculous Infection.— 
A study of the epidemiology of tuberculosis also teaches that the 
dangers of tuberculous infection depend on the length of time a people 
has been exposed to the disease. Thus, when primitive peoples who 
has never been affected with this disease come into tubercle-laden 
surroundings, they are soon infected and the disease runs an acute 
and fatal course in nearly all cases. This is often the case with savages 
and barbarians brought to Europe or America: They almost invariably 
acquire tuberculosis, and succumb in a short time. The American 
Indians, coming in contact with the whites, and incidentally with the 


1 New York Med. Jour., 1907, 86, 624. 

Tuberculosis among Certain Indian Tribes of the United States, Washington, 1909 
3 Ann. de l’Instit. Pasteur, 1912, 26, 497. 

4 Tbid., 1911, 25, 785. 

5 Centralbl. f. Bakteriol., 1913, 70, 1158. 


74 THE EPIDEMIOLOGY OF TUBERCULOSIS 


tubercle bacillus, are being decimated by the disease which runs an 
acute and fatal course among them, and the same is true of the Negro 
population in this country. 

A drastic illustration has been reported by Cummins! from Egypt, 
where the Sudanese soldier, recruited from tribes among which tuber- 
culosis is practically unknown, is much more liable to tuberculosis 
than the Egyptian soldier who has been raised in a region where the 
disease has been quite common for centuries. In former times slaves 
of the Sudanese race were the cheapest in the market, because it was 
assumed that a large number would contract the disease and die. 


SHO-IH/#_ 5 50 100 0 200 250 3co 350 
White 121.2 


Colored FG2 
SHS —IWD 
Whire 11.2 
Colored 309.0 


Fic. 5.—Mortality from pulmonary tuberculosis in the United States Registration 
Area according to race. (Hoffman.) 


During the recent World War this point was clearly brought out 
when African and Asiatic troops were transported to Europe in large 
numbers. S. Lyle Cummins? reports that there were more deaths 
from tuberculosis in the British armies in France during 1917-1918 
in a few companies of Africans than among the whole of the British 
troops in France. The contrast between the case mortality was equally 
striking: 5.7 per cent among the British and 56 per cent among the 
Africans. These African labor units were subjected to careful medical 
examination before leaving their country, which shows that they had 
acquired tuberculosis in France. The Fijian labor units had to be 
repatriated on account of the prevalence of tuberculosis among them. 
The Indian divisions in France during 1916 showed a tuberculosis 
incidence of 27.4 per 1000, as compared with a case incidence of 1.1 
per 1000 among British troops. Similar conditions were observed 
among the Indian and Chinese labor contingents. A. Borel* reports 
the same among the French African troops. He found that among 
those who recently arrived from Senegal only 4 or 5 per cent gave 
positive cutaneous reactions, indicating that they were hardly tuber- 
culized. But after staying in France for some time the death rate 
from tuberculosis increased to 11.14 per cent. On the other hand, 
American negroes, who had been exposed to tuberculous infection in 
the United States, did not show an excessive tuberculosis mortality 
while serving in France with the American Expeditionary Forces. 


1 Tr. Soc. Trop. Med. and Hyg., 1911-1912, 5, 245. 
2 Internat. Jour. Public Health, 1920, 1, 137. 
3 Ann. Inst. Pasteur, 1920, 34, 105. 


SUSCEPTIBILITY TO TUBERCULOUS INFECTION 75 


This is exemplified again by conditions observed among the immi- 
grants to the United States. The Irish and Sicilian immigrants, and 
to a lesser extent the Hungarians, Slavonians, and Scandinavians, 
mostly hail from agricultural parts of their native countries where they 
have known very little of tuberculosis. In this country, working in 
closed factories, and coming in contact with tuberculous fellow-work- 
men, many soon contract the disease, which runs an acute course, 
terminating fatally in a large proportion of cases. Among immigrants 
coming from countries or cities where they have been exposed to 
infection for generations, as is the case with the English, Germans, 
and especially the Jews, the rates of tuberculous mortality are much 
lower. 

When speaking of race influence on the incidence and mortality 
from tuberculosis, the facts just mentioned must always be borne in 
mind. ‘Tuberculosis appears not to be a racial problem—there are 
no races which are more or less vulnerable to the disease, because of 
their ethnic peculiarities, such as height of the body, color of the skin, 
eyes and hair, or other somatic or morphological traits which distin- 
guish one race from another. One human race, or ethnic group, when 
first meeting with tubercle bacilli, is as vulnerable as another. It is 
only after they have been exposed for many generations to the disease 
that they acquire a certain resistance against infection, which, though 
occurring in almost everyone who has been exposed to infection, is 
less liable to cause disease than in races which present virgin soil to 
the bacilli. The mechanics of this acquired immunity will be dis- 
cussed later on. 


Morvratity FROM PULMONARY TUBERCULOSIS PER 100,000 PoPpuULATION. 


1861 1866 1871 1876 1881 1886 1891 1896 1901 1906 


to to to to to to to to to to 

Country. 1865. 1870. 1875. 1880. 1885. 1890. 1895. 1900. 1905. 1910. 
Wuited States... ee Pf ce a Be as bs 171 147 
England and Wales . 253 245 222 204 183 164 146 132 122 111 
megiandme +>.) & ) 202 262 248 229 211 189 174 165 145 
Ireland aaa s We aie 183 191 200 208 212 214 213 215 191 
PAIS OLUG ste lecn x +r Ae nS of 122 121 107 94 8&9 Zhe 
New Zealand Coe See ie are ae 91 84 81 78 70 62 
*QOntario Province . we YH = sf 125 116 114 141 129 113 
(CESS heehee Se * es 361 348 314 224 194 186 159t 
Prussia.) |) nS mn ve are 317 312 290 247 208 191 162 
Bavaria cS ot eeg e a, cs oe ea i% se 287 262 243 214t 
BAxOUVME oe 8 fs we We 251 251 244 236 212 194 154 135f 
Baden a ee er +A we S3 ae 312 297 278 244 PAY 183 
RANISUIIGQG ost a 2f uc eye ee ae 377 393 383 394 345 340 305 
Switzerland . ... nea = os 200 209 213 199 190 189 176¢ 
Netherlands . 2 ah ae Ms sie fy He 189 165 133 125 
eBelgium ) . ....° 805 305 335 323 301 ere 165 142 118 102t 
TANCOR MNS 8 =. = ee as rut ae a 255 249 265 277+ 
Palver yal. Ss a 2% - ie ae 137 100 106 116 123} 
feof hey a er he at 3 a RS es < ees 148 135 
Denmark. << | «> a oe AS 262 249 231 200 160 149 134f 
INGOIWAVS <9. «  . os a 108 126 140 144 173 206 196 200t 
ander. <) S: Ae 374 414 367 255 256 261 273 291 
Serbia ioe sat eee har a 92 A Es ay 251 231 280 297 
*Hungary See pre a ite ar se sig ar 364 397 374 
Chiicmeerr as. |. Gs a2 a nS ar 235 269 
SADAMFeeE cw! aa a oe aE nh 101 136 145 146 154f 


Nortrs.—All figures refer to pulmonary tuberculosis, except those marked * which include all 
forms of tuberculosis. 


Figures in the last column marked } are only for 1906-1908. 


76 THE EPIDEMIOLOGY OF TUBERCULOSIS 


Geographical Distribution.—Sixty years ago Hirsch, in his classical 
study of Geographical and Historical Medicine, arrived at the con- 
clusion that tuberculosis is a disease of all times and all countries. 
With our present knowledge we have not discovered any proofs to 
the contrary. Observations in every part of the habitable globe show 
that the presence or absence of the disease is determined less by 
geographical location, or climatic phenomena, than by social and 
economic conditions and, above all, by the presence or absence of the 
tubercle bacillus. We have shown in the preceding pages that its 
absence in certain countries cannot be ascribed to either an immunity 
of the population, nor to the climate in which they live, nor to the 
altitude on which they have been located. Indeed, it is obvious that 
as soon as the tubercle bacilli are introduced among any people in 
any geographical location, the disease is not slow in making its appear- 
ance. The comparative absence of tuberculosis in the Rockies, the 
Andes, and other mountainous regions, in former times was apparently 
due to the scarcity of population, and the peculiarity of the occupations 
there pursued. In the mountainous regions of the United States 
tuberculosis was scarce before consumptives began to immigrate in 


DEATH-RATES FROM PULMONARY TUBERCULOSIS PER 100,000 PopuLATION IN VARIOUS 


CITIES. 
1881 1886 1891 1896 1901 1906 
to to to to to to 
City. 1885. 1890. 1895. 1900. 1905. 1910. 
Liondonws 5/0) ee Senet Ue eos 197 185 175 157 132 
Abfobbnowvidedsy © Wy Me ene ne) BAY 191 180 187 157 114 
Glasgow: 2. oe Le 250 227 195 170 140 
Dublin y 2.) se eee sO 341 Sap 317 309 268 
Belfastis you. eee Oe 402 382 329 307 235 
iIPATIBGs.- <) i, Be ee eee 440 409 379 390 374 
Berlin cease) .aet eee a ar ne Ee aA 188 
Hamburg. 3 ee 7 me 238 200 169 137 
Miunichee) 3) a eure SSO 348 ols 303 269 226 
Dresdensas., .cfe, fone TOLO 334 283 247 224 180 
Breslawrees om | saeeee ool Sls 342 aA 318 PAHs 
Amsterdam. <)}-0 ane seo 234 204 185 144 138 
Rotterdam | Seen see Lo 192 188 170 133 127 
bhe- Hague. Deka.) pal OD 179 163 160 128 124 
Vienna ">" =2)@.. Breer 685 576 A74 381 336 274 
Prague: gies) aa 2 609 512 472 525 385* 
Budapest 2. ot eee ako 591 434 376 367 340 
‘Trieste: =a ioe ole 491 439 402 396 369 
Christians gee EO LO 287 282 274 229 183* 
Stock Doliisen cee ser enn 44. 303 269 246 227 230 
Copenhagen ... . =. 273 246 198 180 144 136 
Petrograd aed a OO aT 449 384 321 305 301 
Moscoweeey Lo. one ee ET 393 391 324 268 258 
Willan 2V ee "0s. ie ee Cor 307 284 204 232 220 
APUPID some me scant 4h Bien a O40) 222 250 234 225 183 
Syvaney ar) Speen eae OS 157 119 98 98 72 
Melbourne Sie) 2 233 213 182 153 139 109 
Momntreslice eee. cee Se 256 235 250 197 163* 
HLOTONtO Geter tee ae), 207 242 234 174 
RiGLde ganecico, we ee BEALS an 446 A474 455 A402 


Figures marked * indicate that the death-rate in the last column is only for 1910. 


INCIDENCE AMONG RURAL AND URBAN RESIDENTS 77 


search of health. Brown, investigating conditions in El Paso, Texas, 
found that the testimony of physicians is to the effect that deaths due 
to this disease are rare among the indigenous population; E. A. Sweet! 
finds this to be true of the entire southwest region of this country, 
and Cattermole confirmed it in Colorado. But it appears that the 
infection of people living under good sanitary, and above all, economic 
conditions does not always produce phthisis, especially in regions 
where outdoor life is the vogue. 

Incidence among Rural and Urban Residents.— Of greater influence 
than climate and altitude appears to be life in the city, when com- 
pared with life in the country, as regards the morbidity and mortality 
from tuberculosis. It appears that country dwellers, while not exempt 
from infection with tubercle bacilli, are less likely to suffer from 
phthisis than city residents. ‘Thus, the average death-rate from 
tuberculosis of the lungs in the registration area of the United States 
during the decade ending with 1909 was 154.7 per 100,000 population, 
but in the cities of the registration area the rate was 177.4 against 


Urban and Rural, 1900SG19 
Orginal Registration States 
S900-190E Qo 50 s00 430 
Urberr 1834 
Rure! 30.5 
IGIE-SYWD 
lLreen 1354.4 


Rural 104.4 





Fre. 6.—Mortality from pulmonary tuberculosis in the United States Registration 
Area among city and country dwellers. (Hoffman.) 


a rural death-rate of but 124.1. These differences would be even greater 
if we included the rural centers in which factories, mills, mines, etc., 
are located and where the workers live to all intents and purposes 
under the same conditions as those in the cities. Such differences in 
the mortality from phthisis are found in every country where vital 
statistics are gathered. In England and Wales the mortality per 
million population was in 1913: London, 1335; England and Wales, 
1004; rural districts, 742; all urban districts, 1075. The table on page 
76 shows the high mortality-rates from this disease in large cities in 
various parts of the world. When compared with the rates for the 
entire country, as given on page 75, the differences are clear. 

The establishment of sanatoriums for consumptives in rural districts 
during recent years has apparently increased the mortality from this 
disease in certain country districts. Thus, in 1910 the death-rates 
from pulmonary tuberculosis in the State of New York were: in cities, 
165.7; in the rural districts, 120.1, while in Colorado, the Mecca of 


1 Public Health Reports, 1915, 30, 1059, 1147, 1225, 


78 THE EPIDEMIOLOGY OF TUBERCULOSIS 


American consumptives, the rates were: cities, 288.2; in rural districts, 
155.9. It is thus evident that with superior climate and altitude, 
Colorado has a higher mortality from pulmonary tuberculosis than 
the State of New York. Of course, the reason is that most of the fatal 
phthisis in Colorado is imported. According to H. B. Whitney! the 
Coloradoans are practically immune to tuberculosis. He brings statis- 
tics showing that only a small percentage of deaths from this disease 
occur among the natives of Colorado. 





Fia. 7.—Decline in the mortality from pulmonary tuberculosis in American cities 
since 1870. (Hoffman.) 


Wherever available, statistics show clearly that there is more fatal 
tuberculosis in cities than in the country. The reasons for this dis- 
parity should be sought not only in the outdoor life which country 
dwellers indulge in more than city people, but more in the difference 
in social and economic conditions. 

The higher mortality from phthisis in towns as compared with 
rural districts appears to affect only the male population, as has 
recently been shown by Benjamin Moore.2 In the country districts 
of England and Wales it appears that the mortality of females is 
higher than that in the cities. In both town and country nearly 
twice as many girls as boys die from phthisis between the ages of 
ten and fifteen. While until the twentieth year the mortality from 
pulmonary tuberculosis of both sexes is greater in rural districts than 
in urban districts, between the twentieth and thirtieth years the con- 
dition in the towns become reversed. After the thirtieth year the 


1 Colorado Medicine, 1919, 16, 268. 
2 Lancet, 1918, 2, 618, 


INCIDENCE AMONG RURAL AND URBAN RESIDENTS 79 


disease preponderates greatly among urban males as compared with 
urban females. Moreover, the disparity of the phthisis mortality just 
mentioned is a recent phenomenon; it was not observed in the returns 
of seventy years ago. It is apparently due to the recent changes in 
the social and economic conditions of the population brought about by 
the recent conditions among the working classes. 


Mortauity FROM PULMONARY TUBERCULOSIS IN AMERICAN CitTIEs, 1900 To 1919. 
Rates PER 100,000 PopuLaTtion. 











1900-04 1905-09 1910-14 1915-19 

Atlanta, Ga. 5, OS A che Cane ead habe 245.5 193.7 148.9 174.0 
Baltimore, Md. Pe ie eth Lan ae ke. 23000 233.9 204.5 174.5 
(pyemabayed aay eM Ela xe ake Mice GAEL Ger AR lak) Be Vien ae gh Peibetoks 2 22 A. 183.8 
IBOSCOM Me VLAGRte eee ok oo) kn ee Ge PP BY eed 180.9 156.6 151.9 
LSaatehes Yom (fake yA 5 ew ee <4 oe 183.9 162.5 108.6 129.0 
BUlLOmMINGY kere ome On gare! Ge. oa ilps}? 126.6 129.5 Ly oo 
Gamibriace, NEASS: 0.) sere oe ees eae Sih a ee 207.6 224.9 191.4 186.0 
Chicago, Ill. ‘gece fo. 4 Lo yee 157.8 163.7 146.8 130.3 
Gleveiand, Ohio, «$2 un Sia a cae ee | 522258 19720.4) 11858 126.3 
Columbus, Ohio Ae et ye ee 203.6 178.7 if il, ey 128.2 
IDEN Aan Wolsey, 2. F Shek Shel Raed Se ee 184.0 191.0 136.9 119.9 
Denver, Col. Pa ey pee eee 378.0 363.0 274.6 ZOO sey 
Detroit Viichia =) ae a ee ee ee LE Lis20 96.2 88.3 96.9 
Ball aRiver. Maes enue ie fe oA cep 181.8 139.7 139.5 149.8 
GrandihapldswViiCchbier ola ete 8S 105.4 82.8 Gina 74.1 
(ridiarapolige (nC: giae = ame eA A ee a oe 192.8 184.7 167.1. | 149.2 
Nerday: City. aN Wacko oer ee fence Ys § Daone 208.4 | 155.5 139.7 
Mossanreless.@aluaeeas te ako Gore, es. Gs | 320.8 AWE Ae TDR UME 192.9 
ATOUISVI Lem ey ce Aan e Ue Rew te ee a, Pan 1 ts ZOl at 195.4 166.1 
WoawellswViass.me ol Mkt eo ie fece . ors TSOOSL 139.6 107.5 115.7 
Wem DhISt Len ameter a we Gem Ns aech ue 229.8 D202) 2421 Zale 
MalwatlkeetnVVis-s MemeeN Bo ce Ak ect Gem ae 128.7 Wires 98.3 82.5 
Minmenpolsm Vinh: ees sce wee yee 114.9 106.0 122.2 119.0 
Nasivilewlenie =. 4 9s.  o8 -. 303.2 246.9 197.9 178.9 
INEWEKSRNGEC eee Ete cole tele) 239.4 222.8 | 173.5 149.2 
New Haven, Conn. S.A oe ee re: 177.6 164.3 | 118.8 99.0 
NewaOrleang, laren 8 8. ose 324.2 PA ET 252.8 264.0 
INGWEYOLK INS Ls ce ce ba 9. eV Be Dols 202.0 181.0 16065 
Opicignite ba GEES” (5 0) 20 ane ee er a se 16204 158.5 LI226 108.6 
EM USOTIEIN 4 Ute Wenete o tel dust Ss ks ee 188.8 163.7 141.6 128 .2 
Einvagelphiay Pa... .  « « a «- 214.9 207.8 178.0 168.8 
Pittsburgh, Pa. ; ee Ake Oye Taare 120.6 106.4 120.6 
OTA GMOTC. seen ot a Soe eal se oe 107.7 86.9 77.9 YpPadt 
HaroOmaenceyary. Ds. c eilae ogo a 0k 8 a os Zilsicd Ti5e3 130.1 129.8 
ACUMIONGS Var come ty tie ee pre ele 266 . 4 224.8 200.5 INP rf 
I@eneRierieN. Ye. «) wea se AOR Le. Wests its! 136.4 105.0 89.0 
San Francisco, Cal. ee 2 ee a) Sie 279.5 191.8 169.0 164.3 
DINE OI ba) ee a EPR ee | om ce 96.1 81.6 86.4 78.4 
motElo MV Ashita eet coe ac, rk ee 99.0 CCE 86.9 65.5 
Spokane, Wash. Sn oS ae Lae, 94.0 80.1 62.0 
PIOUS wm VLO@ sored) oo 4S <te ge eee, © 196.3 187.1 146.1 125.4 
St. Paul, Minn. 2) OR oe Bl a 108.8 106.6 115.0 iS 159 
Syracuse, N. Y. we ret ee: key 142.3 117.8 97.3 80.2 
Washington, D. C. Sal hh ae as: 274.8 Basel 205.8 160.8 
WMOTCESTGrAVLASS. « = Gf woos om) 180.0 147.9 110.4 118.8 
toe = eS aa ee a) eee 198.9 181.5 158.9 145.1 




















PIDEMIOLOGY OF TUBERCULOSIS 


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SOCIAL AND ECONOMIC FACTORS 81 


Social and Economic Factors.— There is no question but that infec- 
tion with tubercle bacilli is to a large extent influenced by social and 
economic conditions; but it appears from available evidence that the 
development of phthisis is almost altogether dependent on these factors. 
Thus, we find among the so-called well-to-do, the cutaneous tuber- 
culin reaction only rarely reveals hypersensitiveness in infants and 
children. Schlossmann even says that a positive skin reaction is hardly 
ever found in the children of his rich clientele, indicating that they 
are free from infection. The experience of American physicians 
appears to be the same effect, though we do not have data about 
inoculation of a large series of well-to-do children in this, or any other, 
country. It is, however, a rule among pediatrists to place great 
reliance on the tuberculin test in children. That this is justified in 
the case of infants of prosperous parentage may be true, but whether 
in older children a positive skin reaction is exceptional is open to 
question. When children attend school, and later when they go out 
into the world, meeting all sorts and conditions of men, they are no 
longer sheltered against infection, and most of them, in fact, do become 
infected sooner or later. 

The high proportion of positive reactions obtained among children 
and adults in rural districts in Germany and Scandinavia, where 
infection has taken place despite the absence of known open cases of 
tuberculosis, and even where bovine infection could be excluded, 
appears to confirm this view. In fact, it is very rare to find an adult in 
a large city who does not show a positive skin reaction to tuberculin, 
irrespective of his social or economic condition. 

Among the millions of proletariat in large modern industrial cities 
infection appears to be most rampant. Reliable tests—autopsies and 
tuberculin—have shown that very few escape infection, and the 
clinics, sanatoriums, and hospitals for tuberculous patients derive their 
clinical material mainly from these strata of population. A study of 
the mortality-rates also shows that these are the people who are most 
likely to succumb to tuberculosis. One has only to glance over the 
maps of New York City prepared under the auspices of Herman M. 
Biggs to be convinced that poverty and tuberculosis go hand-in-hand. 
The blocks inhabited by the rich show exceedingly few deaths from 
this disease, while those inhabited by the artisans, the laborers, and 
the poor—the “slums’”’—are appallingly studded with cases of phthisis. 
Poverty, filth, and overcrowding may act by favoring the spread of 
infection, or by reducing the inherent resisting powers. 

Illustrations from other cities are not wanting. In Hamburg the 
death-rates from tuberculosis are in inverse ratio to the amount of 
income tax paid by the various groups of population. In Paris, Ber- 
tillon found that in the very rich district Elysée the mortality from 
tuberculosis is the least in the city; it is somewhat higher in the rich 
Opera district; higher in the very well-to-do district Luxembourg; 
higher yet in the well-to-do Temple district; very high in the peor 
Reuilly district, and highest in the Twentieth Arrondissement, where 

6 


2 THE EPIDEMIOLOGY OF TUBERCULOSIS 


the inhabitants are exceedingly poor. In Glasgow, according to 
Glaister, the mortality is higher among families living in one-room 
apartments than in those who live comfortably in several rooms. In 
Edinburgh, A. Maxwell Williamson! found that the number of cases 
of tuberculous disease increases in proportion as the house accommo- 
dations become limited. “ Pulmonary tuberculosis is a disease which 
in 70 to 80 per cent of cases occurs in houses of three rooms and under; 
the number of cases is larger in two-room houses than in three; larger 
in houses of one room than in two; and the number of cases of the 
disease increases almost in direct proportion to the number of small 
houses in any district or ward of a city.’’ The relation of phthisis to 
overcrowding is seen clearly in the industrial cities of the United States. 

Similar investigations as to the relations of wages to morbidity and 
mortality of tuberculosis have shown that higher wages mean less 
of the disease (see p. 89). The experience of life insurance companies 
is to the effect that industrial policyholders, who pay small weekly 
premiums, are more likely to succumb to the disease than those who 
hold “ordinary” policies paying annual premiums. In Europe it has 
been observed that the larger the amount for which the person is 
insured, the less likely he is to succumb to tuberculosis. 

The influence of poverty, with its concomitant poor nutrition, on 
the incidence of tuberculosis has been demonstrated recently in the 
countries affected by the war, directly or indirectly. The mortality 
increased wherever the cost of living went up—in Germany, Austria, 
France, England, etc., and also in the Scandinavian countries, in 
Holland, in Brazil, and Argentine. Scarcity of nourishing food, and 
its high cost, producing undernutrition even in those who ordinarily 
have plenty, is undoubtedly the agent. In Germany, and especially 
in Austria, the tuberculosis mortality rose to an appalling degree dur- 
ing the World War, and reached its apex during the eighteen months 
following the conclusion of peace. But as soon as economic conditions 
improved, food becoming less scarce, especially as soon as fat was 
procurable, a remarkable and prompt improvement took place and the 
death-rates declined, tending toward those that prevailed before the 
war.) In England and Wales the following figures, taken from the 
Registrar-General’s Reports, show the effects of the hardships of the 
war on the tuberculosis mortality: 


Morvtauiry PER 1,000,000 rrom PuLMONARY TUBERCULOSIS. 








1912-14. 1915. 1916. 1917. 1918. 1919. 
Males: 2): 6e8 at. atti aect yes 1179 1487 1624 1885 2077 1116 
Females We ee NR Oe oe 849 912 913 969 1055 842 
All ae Ae eee ae 1005 1185 1252 1406 1543 971 























1 British Jour. Tuberc., ED LOR O pelle 
“1 See especially Selter and Nehring, Ztschr. f. Tuberkulose, 1921, 34, 1; Rosenfeld, 
Die Aenderungen der Tuberkulosehiufigkeit Oesterreichs durch den Krieg, Vienna, 1920. 


INFLUENCE OF AGE 83 


The tuberculosis mortality increased between 1915-18, but sharply 
declined so that in 1919 it came down to a little below that which 
obtained in 1912-14, before the war. Similar conditions were observed 
in the city of Paris during the Siege in 1870-71 in an even more 
accentuated form. 

The slums of large cities contain “lung’”’ blocks which have been 
pictured in such sombre colors in the popular tuberculosis literature. 
Of course, the bad housing conditions are responsible to a large extent. 
But it must be remembered also that “a slum is not constituted solely 
of broken-down houses, but also of broken-down occupants, and it is 
perhaps easier to remedy the one than the other,” says John Glaister.! 
Moreover, the tuberculous, unable to earn a living, are more likely to 
move into cheap, 2. e., unsanitary, dwellings. This is a factor which is 
not generally appreciated when slums and “lung blocks” are spoken of. 

Thus, we have a vicious circle in the economics of tuberculosis. 
Poverty brings about congestion and overcrowding, enhancing the 
chances of massive infection; it also compels its victims to work in 
unsanitary factories, mills and workshops and at trades which are 
dangerous in this regard. The vitality is depressed and the powers of 
resistance reduced as a result of insufficient and improperly prepared 
food, so that infection more often terminates in phthisis than among 
those who are higher in the social scale. 

However, that the well-to-do and rich do not escape is evident when 
we glance into the modern private sanatoriums, which derive their 
clientele from those who can pay more than fifty dollars per week, 
not including medical attendance. The resorts in Europe are also 
filled with rich consumptives, as can be seen in Switzerland and the 
Riviera. Of course, this shows that not all well-to-do individuals 
live wisely, even though they can well afford to do so. 

Influence of Age.—In considering the influence of age on the inci- 
dence of tuberculosis we must again differentiate tuberculous infection 
from morbidity and from mortality, and also the various forms of the 
disease. 

The newborn infant is free from tuberculosis, as we have shown; 
infection takes place during the lifetime of the individual who is exposed 
to the bacilli. We have already seen that those living in a tuberculous 
milieu do not escape, and during the first year about 15 per cent are 
infected; during the first five years, about 50 per cent, and at the age 
of fourteen, over 80 per cent are infected. Even children of non- 
tuberculous parentage are infected with tuberculosis to the same 
extent as those of tuberculous stock, but not at such an early age, 
and when reaching adolescence the difference is not so pronounced 
as would be expected a@ priort. 

The morbidity from the disease is greatly influenced by age. During 
the first two years of life tuberculosis is very frequently encountered 


1 Practitioner, 1913, 90, 344. 


THE EPIDEMIOLOGY OF TUBERCULOSIS 


84 


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INFLUENCE OF AGE 85 


and chronic pulmonary tuberculosis is very rare. Only after the age 
of ten does the latter form of tuberculosis make its appearance, and 
after fifteen years of age it becomes the menace of society—the pro- 
verbial “white plague” —causing more misery than any other disease. 

The disease is, however, for lack of reliable morbidity statistics, best 
gauged by a study of the mortality-rates. From the table below 
it is seen that there are two maximums of mortality. The first during 
the first two years of life; while beginning with the third year, tuber- 
culosis becomes a very infrequent cause of death until the tenth year 
is reached, when it again begins to rise, reaching its full height at 
twenty years, and keeps at that high level with slight fluctuations 
until sixty years, when there is again a slight decline. 


MorTALity FROM TUBERCULOSIS IN THE REGISTRATION AREA OF THE UNITED 
Srates PER 10,000 Livine at THE GIvEN AGE AND Sex, 1910-1913. 


All other forms of 


Pulmonary tuberculosis. tuberculosis. 

Age. Males. Females. Males. Females. 
Oltpr Ls Gavia 5.68 13.76 12.14 
jes 4.72 4.00 hiss 10.64 

Pes 2.14 1E9E 6.13 5.53 

oie 1.44 1.41 3.95 3.84 

4, 1.00 LetG 2.90 2.78 

oO). 0.97 0.94 2.10 1.54 

GF: 0.92 0.84 2. Ol easy) 

Wh 0.85 1.19 iets; 1.95 

sae 0.63 1.26° Tao 2.07 

OF. 0.98 Sal retell 2.14 

10 to 14. 1.22 2.94 il 5s) 1.35 
SECO Oe. ewe oS 8 7.96 11.09 Uh eee 2.09 
BORLOUCEEG be) a my LOL 7 17.66 2.10 2.26 
BOLO ZOE Ge wen oo 718.98 19.33 2.12 2.10 
SOMO tune cee mete 2. 70 18.62 2.08 2.01 
335) Oot a ee eg eel 16.22 2.09 1.89 
AUIUOIaEe ee a on cocky 14.25 2.07 1.69 
4s). Gey Gey A ae ec IO 11.99 2.02 Oo 
BUMO.O4). c-s » . ALS LIS 2.04 1.63 
DOCOMO ss cs. oo s, 22.99 11.80 2.47 1.96 
GCUMOLOtiee ss |. 222.43 12.39 2e00 1.92 
Gasono9=. —. « «. . 21.00 14.25 2.45 Die Qe 
MOMOk4 oe sa =e « 20.11 Loc 2.68 250k 
BOELORLONee =. 9. 2 « 18302 16.07 2.41 De TAY) 
BULOsS4t es oe 13. 64. : 13.24 2.02 PAR AD) 
SOmOLSoue ys oo . . 12.48 10.23 2.38 2.23 
OORtO 947, 95 4 =: 9.71 6.58 Lei 1.25 
pormandcover. = = . LO.d7 Gril al 5)” 


It is thus clear that the rate of infection with tuberculosis does not 
follow closely the rate at which the disease kills. As shown in the table on 
page 71, infection begins during the first year of life, keeps on increasing 
during every subsequent year until at the age of twenty very few indi- 
viduals are found who have escaped it. The mortality is comparatively 
high during the first year of life, but then declines, so that between 
three and twelve years, just the period when most infections occur, 
the number of deaths is the least, and only after the fifteenth year does 


86 THE EPIDEMIOLOGY OF TUBERCULOSIS 


the mortality rise to its highest point, and keeps at it throughout life. 
The bearings of these facts on the problems of phthisiogenesis and 
prophylaxis will appear in other sections of this book. 





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Influence of Sex.—I*rom the table on page 85 we find that during 
the first six years of life the mortality from pulmonary tuberculosis 
is somewhat, though not very materially, less among females than 
among males. After the sixth year the rates among females are higher 


INFLUENCE OF SEX 87 


than among males of the corresponding age groups. Between fifteen 
and thirty years of age the difference in favor of the males is striking. 
After thirty years the females again show lower mortality-rates which 
keep up until the end of natural human life. The total mortality is 
less among females than among males, a fact which has been observed 
in all countries where vital statistics are available. In New York 
City the mortality from phthisis in 1920 was: Among the total 
population 11.9 per 10,000; among males 14.9, and among females 
only 8.5. 

Various explanations have been offered for this disparity in the mor- 
tality from phthisis between the two sexes. It has been suggested that 
the more hazardous occupations, in which men are mainly engaged, 
reduced their resistance, and predisposed them to phthisis; or when 


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Fia. 11.—Death-rates per 100,000 population by age and sex in the Commonwealth of 
Australia for the years 1909-1913 (all forms of tuberculosis). Males, 
HETINR ICR e en (a Si scscie 





becoming sick with the disease, the chances of recovery are less in 
the case of men who have to work for their support, as well as for 
those depending on them. But during the ages of fifteen to forty-five, 
when menstruation, pregnancies and lactation undermine the resisting 
powers of women, it would be but natural that the mortality from 
phthisis should be high among them. Vital statistics in some countries 
seem to support this view, but in the United States and in the Com- 
monwealth of Australia (Fig. 11) the higher mortality among the 
women keeps up only until the age of thirty, when it again declines as 
compared with the men. 

It appears to me that the higher mortality from phthisis among 
women between fifteen and thirty in the United States is to be attrib- 
uted to the large number engaged in gainful occupations. This is con- 


er, without regard to 


among all classes of popula- 
occupation, the proportion of deaths from tuberculosis is 56 per cent 


THE EPIDEMIOLOGY OF TUBERCULOSIS 


tion, male and female, ten years of age and ov 


firmed by the census returns showing that 


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INFLUENCE OF SEX 89 


males, and 44 per cent females. When women enter gainful occupations 
to earn a living, as B. S. Warren! has shown, the proportion is reversed 
and the difference much greater. Thus, among salesmen tuberculosis 
constitutes 15.8 per cent of all deaths, as against 31.1 per cent among 
saleswomen; among silk-mill weavers, men 19.7 per cent and women 
38.3 per cent; among woollen-mill operatives, males 22.2 per cent and 
females 29.2 per cent; clerks and copyists, males 29.2 per cent and 
females 31.8 per cent; and boot and shoemakers, males 13.3 per cent 
and females 31.8 per cent. It thus appears that it is more a problem 
of industrial conditions than of sexual differences. In fact, women 
do not bear hard work under deleterious conditions as well as men, 
and succumb to phthisis in greater numbers when, in addition to 
exercising their physiological functions, they become bread-winners. 

Since women entered industrial occupations, their mortality from 
tuberculosis has greatly increased. Thus, in Stockholm, the mortality 
from tuberculosis since 1881 has been in women only two-thirds that 
of men. E. Lindhagen? shows that between fifteen and twenty years 
of age the death-rate in women has, however, increased by 18 per 
cent, while that of men has been reduced by 12 per cent. During the 
World War there was noted an increase in the tuberculosis rates 
in females much more intense than that of the males. Conditions in 
England are given in the table on page 82. 

In the Netherlands similar conditions have been observed. B.H.Sajet* 
shows that in cities the tuberculosis death-rates have increased since 
the war from 154.4 per 100,000 in 1913 to 175.9 in 1916. The mor- 
tality has, however, not increased materially among young men in 
the cities, but there has been noted a great increase among the women 
between twenty and thirty years of age, 7. e., among those of working 
age. This is, perhaps, best shown by conditions in Vienna, where the 
effects of the war have been most disastrous. According to Sigismund 
Peller! the mortality from tuberculosis before the war, in 1913-14, 
as compared with 1919, after the war was as follows, per 10,000 popu- 
lation: 


Men. Women. 
OS Ae reg EIR a Shel yr 1 Se Ra oS eee OTD 24.8 
To ee fn re) ae See er ee 4. D eo) 


The increase in the mortality of the women is thus seen to have 
been 110 per cent, while of the men, 54 per cent. Similar conditions 
were also observed in other belligerent countries, and in_ those 
in which the labor market was affected by the war, though not to 
such an appalling extent as in Austria, Serbia, Poland, ete. It was 
not only the reduced food supply and the increased cost of living that 
was responsible for this increase, but also the fact that women, who 


1 Tr. Nat. Assn. Study and Prevent. Tuberc., 1913, 9, 153. 
2 Hygeia, 1918, 80, 497. 

3 Nederl. Tijschr. ven. Genaec., 1917, p. 1859. 

4 Wien. klin. Wehnschr., 1920, 33, 906. 


90 THE EPIDEMIOLOGY OF TUBERCULOSIS 


formerly were idle, or engaged in less dangerous trades, had to 
go to work at all kinds and conditions of labor, and thus their mor- 
tality from the most important of industrial diseases increased. 

Mortality-rates from Pulmonary Tuberculosis.—It is impossible 
at present to give with certainty the extent of tuberculous morbidity 
in any population. Even in cities where registration of this disease 
is compulsory, the data collected in this manner are not complete, 
and we do not know the exact number of persons suffering from active 
tuberculosis. The statistics published by certain benevolent and indus- 
trial societies are also inconclusive because they concern only certain 
groups of people, and the results cannot be applied to the general popu- 
lation. Attempts have been made to ascertain the morbidity-rates 
from tuberculosis by multiplying the number of deaths occurring 
in a given region by the average duration of the disease. Thus, there 
annually occur about 150,000 deaths due to tuberculosis in the United 
States; in Germany, over 100,000; in France, 70,000; in England and 
Wales, over 50,000, ete. But attempts at multiplying these numbers 
by the number representing the average duration of the disease and 
thus finding the actual number of sick have met with failure because 
there is no agreement as to the average length of phthisis. Indeed, 
it has been estimated at from one to ten years by different authors. 

The extent of the disease is therefore best gauged by the number 
of deaths it causes in a given population. The table on page 75 gives 
the mortality per 100,000 population in different countries. When 
in connection with these figures we bear in mind that one-third of 
all the deaths during the prime of life, between fifteen and forty, are 
due to tuberculosis, of which over 90 per cent is phthisis, we realize 
the enormity of the problem presented by tuberculosis and the reason 
why it has been considered the most important of diseases with which 
humanity has to cope. 

Statisticians are, however, inclined to question the accuracy of the 
tuberculosis mortality statistics. Some state that many persons dying 
from other pulmonary diseases, notably bronchitis, pneumonia, typhoid, 
cerebrospinal meningitis, influenza, etc., as well as many other diseases, 
which occur in consumptives as often as in others, are reported as 
having died from these diseases, though the real cause of death was 
undoubtedly phthisis. This point is well illustrated in the mortality- 
rates in Italy. During 1896-1901 only 1060 per million died from 
tuberculosis in Italy as against 1911 in Switzerland. But in Italy 
during the same period there were reported as having died 2032 from 
bronchitis, 2031 from pneumonia, and a total of 4641 deaths per 
million from various diseases of the respiratory organs. In Switzer- 
land during the same period the rates were: Bronchitis, 1092; pneu- 
monia, 1525, and all respiratory diseases, 2828. Similar figures may 
be culled from the Registrar’s Officers’ reports in many other countries. 
This is also to be seen from the fact that in cities in which compulsory 
registration of tuberculous patients is enforced, a large proportion 


DECLINE IN THE MORTALITY FROM TUBERCULOSIS 91 


who are reported tuberculous are in the end certified as having died 
from other diseases, which is undoubtedly true, because tuberculous 
patients are liable to other fatal diseases, but still, while alive, they 
were tuberculous and sources of infection. It has been my observation 
that in populations in which so-called “industrial insurance”’ is com- 
monly taken out by the poorer strata of the people, tuberculosis is 
often not given as the cause of death, because it may interfere with 
the collection of the death claims from the insurance companies. It 
is also a fact that since tuberculosis has become an actual stigma, 
some deaths due to this disease are returned as having been caused 
by other diseases with a view of sparing the families the feeling of 
“tainted blood.” 

The differences in the mortality-rates for the various countries are 
due to diverse causes, mainly the intensity of concentration of popu- 
lation in cities, the character of the occupations pursued by the people, 
and other factors which have already been discussed. 

Decline in the Mortality from Tuberculosis.— Another point brought 
out by the figures in this table is that the mortality from tuberculosis 
has been declining in nearly all countries where statistics are available, 
excepting in Norway, Ireland, Serbia, Spain, France, Italy, Japan, 
Hungary, etc. This decline is of great significance, and if the exact 
causes were ascertained we might be in a position to accelerate it, so 
that ultimately the disease could be stamped out altogether. 

In England the decline in the tuberculosis mortality can be traced 
back for 150 years. “In the years 1743-53,’ says Arthur Ransome,! 
“when, as Ogle says, ‘there were fairly accurate transcripts from the 
parish registers, the proportion of deaths was rather more than one- 
fifth; and, in the first returns of the Registrar-General, in 1838, in 
London, it was | to 6 or 8.’ In other words, the rate per thousand 
deaths in the former period was about 200, and in the latter about 
148. Hence, in the middle of the eighteenth century, phthisis must 
have been still more common than in 1838; and then the diminution 
in the mortality from the disease must have been proceeding steadily, 
at about the same rate as that observed in the earlier years.” A 
glance at Fig. 14, showing the mortality in 1851-70, as compared with 
subsequent decennia to 1910, proves conclusively that the mortality 
has declined. The same is true of Scotland, Australia, Germany, 
Austria, etc. For the United States Frederick L. Hoffman’s? statistics 
(see Fig. 13) tend to show that the mortality from tuberculosis in 
New York, Philadelphia, Boston, etc., has been constantly declining 
during the past one hundred years. 

What are the causes of this decline in the tuberculosis mortality? 
All authorities agree that it is mainly due to the causes which have 
been operative in reducing the general mortality; in banishing, or 
abating, the malignancy of most other infectious diseases. Among 


1 Tr. Epidemiol. Soe., London, 1904-05, 24, 259. 
2 Tr. Nat. Assn. Study of Prevent. Tubere., 1913, 9, 101. 


in the 


sanitary and hygienic conditions under which the bulk of the people 
live at present. It is also to be considered that modern factory legis- 


to be considered the improvements 
lation, the improvements in the economic conditions of the people, 


THE EPIDEMIOLOGY OF TUBERCULOSIS 
are largely 


these factors 


92 


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CAMPAIGN AGAINST THE SPREAD OF THE DISEASE 93 


the shorter hours of work, etc., which are characteristic of the present, 
as compared with conditions during the first half of the nineteenth 
century, have been instrumental in reducing the general mortality 
and phthisis as well. Wages have been increasing, and the food 
consumed by the working people of today is much superior to that 
which they could afford fifty or one hundred years ago. The distribu- 
tion of food, as well as its preservation, precludes famines at present. 
An increase in the tuberculosis-rates is often observed during and 
after famines. 









































































































































PER 10,000 
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Fic. 14.—Mortality from phthisis by age groups in England and Wales per 10,000 
living, showing the decrease from 1851 to 1912. Dotted line, mortality during 1851— 
1856; black line, mortality in 1912. 


The Effect of the Special Campaign against the Spread of the 
Disease.— Most authors, when speaking of the reduction in the tuber- 
culosis mortality, point at once at the special measures which have 
been taken to combat this disease as the sole factor in this direction. 
In fact, the figures compiled in the tables on pp. 76 and 79 are always 
brought forward in proof of the effectiveness of the antituberculosis 
‘ampaign which has been so aggressively waged. 

But careful studies of the available statistical data have not sus- 
tained this contention. In England, where the decline has been more 
pronounced than in any other country, it has been shown by competent 
statisticians that such is not the fact. Karl Pearson! points out that, 
examining available data, it appears that the death-rates from phthisis 
are steadily increasing as we go backward to 1838; according to Arthur 
Ransome even as far back as 1743, as was mentioned above. Now, 
this could not go on indefinitely because if it did, every individual five 


1 The Fight against Tuberculosis and the Death-rate from Phthisis, London, 1911, p. 9. 


94 THE EPIDEMIOLOGY OF TUBERCULOSIS 


hundred years ago must have died in England from phthisis. There 
was assuredly a time in England when the phthisis rates were rising, 
just as they have recently been falling. “We have to stretch,” says 
Pearson, “our ideas of time a little and we should realize the possibility 
of a typical epidemic curve in the frequency of phthisis. Indeed, the 
mortality from phthisis in England has been declining since 1838, 
7. e., long before any special measures had been taken for the control 
of the disease, or segregation of the sources of infection—tuberculous 
human beings and animals—had been attempted.”’ 

Data from other countries, especially where the disease has become 
a menace during recent years, confirm these views. During the first 
half of the nineteenth century there were isolated areas in Europe 
where tuberculosis was rare, but with the segregation of the popula- 
tion in cities during recent years, and the introduction of modern indus- 
trial conditions, the disease has made its appearance, and rages there 
with greater vigor than in countries where the disease has appeared 
before. Thus, the tuberculosis mortality has been rising in Ireland, 
Norway, Sweden, Serbia, Bulgaria, Roumania, Hungary, Portugal, 
Italy, Japan, etc., during the very period that it has been declining in 
England, Germany, etc. There is no doubt that the measures taken 
for the control of the disease in Norway are as aggressive and advanced 
as those taken in neighboring Denmark, yet in the former the mor- 
tality-rates have been rising, while in the latter they have steadily 
declined. The same is true of France when compared with Belgium, 
and similar analogies can be made between other countries, or various 
regions of any single country. 

The differences in the mortality from tuberculosis in the various 
cities in this country, as shown in the table on p. 79 point in the same 
direction. The various agencies engaged in the campaign against the 
spread of tuberculosis have not neglected the cities of Buffalo, Minne- 
apolis, St. Paul, ete., yet the tuberculosis mortality has increased 
during the past fifteen years, while in others it has decreased. 

It appears that the mortality-rates from tuberculosis have been declin- 
ing to the same extent as the general mortality from all causes, as has been 
shown clearly by many competent statisticians. Professor Walter F. 
Wilcox! says that “to show that the campaign against tuberculosis is 
having its effects, it should be found that the death-rates from that 
disease are decreasing faster than the average for all other causes.”’ 
But a test of this question with statistics for the mortality in the State 
of New York shows that the result is a negative one. ‘“ No influence 
of the special campaign can be traced in the figures. The condition 
in Michigan is similar to that in New York. In Indiana the number 
of deaths in each instance had decreased, but apparently the propor- 
tion of those from tuberculosis to all others has not.” In New Jersey 
and Rhode Island, while the mortality from other causes has been 


! Monthly Bulletin New York Board of Health, 1910, 26, 85. 


CAMPAIGN AGAINST THE SPREAD OF THE DISEASE 95 


decreasing, that from tuberculosis has been increasing, so that the 
comparative proportion of the latter has risen. Pearson! has proved 
incontrovertibly that since the campaign has been waged in England 
against tuberculosis “the rate of fall in the death-rate from phthisis, 
instead of being accelerated, has been retarded.” From careful statis- 
tical studies he arrives at the conclusion that “somewhere about 1915 
the fall in the phthisis-rate which had been less rapid since 1895 would 
cease altogether and probably be followed by a rise. The next five 
years will show whether this is true or not.” 

Statisticians are not alone in this opinion. In a posthumous paper 
by Robert Koch? he states that the special measures taken for the 
control of tuberculosis, such as segregation of consumptives, the erec- 
tion of sanatoriums, ete., are not to be taken as the sole factors which 
have been instrumental in reducing the mortality from tuberculosis 
during recent years. He says: “Many have correlated the decrease 
in the tuberculosis mortality with the discovery of the tubercle bacillus. 
It. was stated that since proofs have been produced that tuberculosis 
is transmissible, greater care has been taken to prevent infection, 
while before the discovery of the tubercle bacillus, physicians, and 
with them the laity, denied the transmissibility of the disease. This 
assumption surely has something in its favor. At any rate, it is a strik- 
ing fact that, with but few exceptions, the decline in the mortality 
began a few years after the discovery of this bacillus. But just these 
exceptions prove that the newly engendered fear of the dangers of 
infection is not the only factor operative in this direction, although 
we must give it a certain, and not an inconsiderable, amount of credit. 
Among German authors we often meet with the view that the recent 
social legislation, especially that concerning workmen’s insurance, has 
been effective in reducing the tuberculosis mortality. To a certain 
degree there is some correlation in time between these two phenomena 
in Germany. But, inasmuch as in most other countries such laws 
have not been inaugurated and the decline in the tuberculosis mor- 
tality has taken place to the same extent as in Germany, this factor 
should also not be taken as a cause.”’ 

In this country we now hear similar opinions expressed. William 
Charles White® says: “We cannot possibly avoid the facts that in 
spite of all our labor our results are not what we might have expected 
on a right premise; for our reduction in morbidity and mortality from 
tuberculosis has not kept pace with the reduction in the general 
death-rate; and, further, our reduction in mortality was about as great 
before we started our present methods, and in proving how great the 
influence of our efforts has been we usually neglect all the influences 
‘that operated before we began, and new factors, such as the Mills- 
Reinecke phenomenon, and ascribe all good to our own work.” Like- 


1 Biometrica, 1918, 12, 347. 
2 Ttschr. i. Hyg.; 1910, 67, 1. 
3 Tr. Nat. Assn. Study and Prevent. of Tuberc., 1913, 9, 80. 


96 THE EPIDEMIOLOGY OF TUBERCULOSIS 


wise, Raymond Pearl,! one of the ablest biometricians in this country, 
says that the death-rates in Baltimore, calculated for the past ninety 
years, show the same tendencies to rise as was observed by Pearson 
to be the case in England. About the campaign against tuberculosis 
he has this to say: “When I see millions of dollars literally thrown 
away each year on charitable and public health activities—which every 
trained geneticist, if he used the analytical powers of his mind to the 
same good purpose that he does in his laboratory, could demonstrate 
to be futile, because of the limitations which known facts of heredity 
place on these well-meant endeavors—I am appalled and disheartened 
at the spectacle science permits to be made of itself.”’ 

Perhaps the best proof of the contention that the decline in the 
tuberculosis mortality during the past one hundred years has hardly, 
if at all, been accelerated by the campaign waged against this disease 
is to be found in the fact that the number of persons infected with tubercle 
bacilli has not decreased. We must bear in mind that modern methods 
of prophylaxis aim mainly at but one thing: The prevention of infec- 
tion. In this we have utterly failed, as could be expected, considering 
the ubiquity of tubercle bacilli “carriers,” and that hardly 5 per cent 
of “open” cases of tuberculosis have been isolated by hospitalization 
in even the most progressive communities. We have shown con- 
clusively that over 90 per cent of humanity harbor tuberculous lesions 
in their badies (see p. 70), indicating that our efforts at keeping these 
organisms from infecting humanity have hardly met with encouraging 
success. 

Causes of the Decline in the Tuberculosis Mortality.— Despite our 
failure to prevent infection, there has taken place a very important 
decline in the morbidity, and particularly in the mortality, from 
tuberculosis during the past one hundred years in some countries, as 
England, the United States, etc.; and in others, like Germany, Austria, 
Holland, Switzerland, ete., during the past fifty years. As far as our 
present knowledge goes, we are not in a position to credit this decline 
to any single known cause; it is apparently due to many, and complex, 
factors which, with our present meager knowledge of phthisiogenesis, 
largely remain obscure. 

Many, especially geneticists, suggest that tuberculosis is declining 
in frequency and fatality in countries in which it has been widespread 
for centuries by a process of natural selection. Pearson looks “upon 
the decline as a result of a pure selective process, the survival of people 
with an inherited immunity in various grades, and not with an acquired 
immunity.” This view is not in conflict with our knowledge of the 
lack of inheritance of acquired characters. Persons with excessively 
susceptible constitutions die, mostly during the early years of life, 
leaving few or none who have inherited their weakly constitutions. 
In favor of this view is the hypothesis that the phthisical constitution 


1 Jour. Am. Med. Assn., 1920, 74, 375. 


CAUSES OF THE DECLINE IN TUBERCULOSIS MORTALITY 97 ~ 


is not a specific trait which predisposes to the disease, but a general 
predisposition, a point which is discussed in detail in Chapter IV. 
The facts presented above (see p. 73) about the deadliness of tuber- 
culosis in communities in which it was not known before, also tend to 
confirm this view. Available epidemiological data tend to show that 
wherever people who have hitherto been free from tuberculosis come 
into tubercle laden surroundings, they succumb to the more acute 
and fatal forms of the disease, while most of those who have for gener- 
ations been tuberculized are either not harmed by the specific germs, 
phthisis not developing after the vast majority of infections, or when 
this does take place, the disease manifests a strong tendency to pursue 
an exceedingly chronic course, or heals spontaneously in the vast 
majority of cases. This point has been discussed in detail in a paper 
by the writer! on “'Tuberculization and Immunization;” more recently 
Bushnell? has published an excellent work on this subject. It seems 
that after contact with the tubercle bacilli for several centuries, the 
human being adapts itself to the conditions created by these micro- 
organisms, which can live in symbiotic relationship with the host. 

Careful studies of the economic and social conditions in the various 
European and American countries in which statistical data are avail- 
able, tends to show that there is a pronounced correlation between 
urbanization, 2. e., concentration of large masses of population in cities, 
and the death-rates from phthisis. Wherever the process of urbaniza- 
tion. is new, wherever modern industrial conditions have only recently 
been introduced, and large numbers of rural people have been attracted 
to cities, the death-rates from phthisis have been rising. This is the 
case in Japan, Norway, Sweden, Ireland, Serbia, Roumania, Bulgaria, 
Russia, Austria, Italy, France, etc., in which countries the death-rates 
from phthisis have either increased during recent years, or have failed 
to decline perceptibly. On the other hand, in England, where indus- 
trial development was already on a high scale at the beginning of the 
nineteenth century, it was at that time that the high phthisis mortality 
occurred, and it began to decline with the increased adaptation of the 
population to city life. In line with this urbanization can be considered 
the conditions of the negroes in the United States. The phthisis mor- 
tality among them is higher than among the whites. Though it cannot 
be said that very efficient measures are taken by them to prevent dis- 
semination of the disease, there has been found a strong tendency 
toward a reduction in the death rates. Thus, in Baltimore, John W. 
Fulton found to his amazement that “both races gained against 
tuberculosis, the whites at the rate of 30.8 per cent, and the negroes 
at the rate of 24.5 per cent, in the decade of 1904-1913.” 

While it cannot be said that social and economic conditions are alto- 
gether responsible for the incidence, or lack, of tuberculous disease, there 
seems to be no doubt that within certain limits they are the determin- 


1 Fishberg: New York Med. Jour., 1914, 100, 497, 566. 
* A Study of the Epidemiology of Tuberculosis, New York, 1920. 


98 THE EPIDEMIOLOGY OF TUBERCULOSIS 


ing factor in a large proportion of instances. There can be made out 
a good case in favor of high wages, which have as their concomitants 
superior housing conditions, better nourishment, etc. (see pp.81 and 89). 
Indeed, in countries in which social and economic conditions of the 
workmen are superior, the mortality from tuberculosis is low and keeps 
on declining. With the improvement in the economic conditions of 
the British and American laborers during the past century, the tuber- 
culosis mortality has decreased. With the misery brought about by 
the World War, the tuberculosis mortality in Austria, Germany, 
Poland, France, England, ete., increased to an appalling degree. 
The increase in the female mortality from phthisis observed in some 
countries, warring and neutral (see p. 89), during that war, may be 
attributed to some degree to the entry of women into factories in 
large numbers. In line with this is the fact that while the mortality 
from this disease increased during the World War in most of the par- 
ticipating countries, in the United States, where food has been abun- 
dant, it declined. However, an association between the economic 
conditions and the tuberculosis death-rates is suggested in the fact 
that immediately preceding the rise in mortality during 1914-1915, 
there was a period of serious unemployment, and that in 1917-1920 
wages kept pace with living costs and the demand for labor was extra- 
ordinarily great... The sharp decline during 1920-1921 has been 
attributed to another factor: In 1918-1919 the epidemic waves of 
influenza carried off many persons who would have died within the 
two succeeding years. In the Report of the Registrar-General of 
England and Wales, Stevenson is inclined to explain the drop of the 
tuberculosis mortality in that country to the same cause. 

At the present state of our knowledge, which is quite incomplete, 
the decrease recently observed in the mortality rates from tubercu- 
losis can be attributed, in great part, to two factors: Mutual adapta- 
tion of the parasite and the host, and improved social and economic 
conditions of the great masses of population. The first has been brought 
about mainly by a process of natural selection, the more susceptible 
succumb to the tubercle bacillus. The second apparently depends 
on the improved social and economic conditions of the great masses 
of population in modern Western European and American urban 
centers. It appears that in well-fed, and properly housed individuals 
tuberculous infection, which is inevitable in nearly all who live in 
modern cities, is less likely to develop into the disease, phthisis, than 
in those who are undernourished and famished. 

Brownlee’s Three Types of Phthisis.—In a very careful statistical 
study of the incidence and mortality of tuberculosis in Great Britain 
and Ireland, John Brownlee? has arrived at the conclusion that phthisis 
pulmonalis is not a single disease, as is commonly understood, but 


1 See Public Health Reports, 1921, 36, 1178. 
2 An Investigation into the Epidemiology of Phthisis in Great Britain and Ireland, 
Medical Research Committee, Special Report Series, London, 1918-1920, Nos. 18 and 46, 


BROWNLELR’S THREE TYPES OF PHTHISIS 99 


rather a group of diseases, in the sense as has been found the case 
with typhoid fever and bacillary dysentery. He brings strong evidence 
in support of his contention that there are three types of phthisis. 
the “young adult,” “middle age,” and “old age’ phthisis. 

The Young Adult Type—The “young adult’ type is the most 
important. It occurs mostly in young adults, twenty to twenty-five 
years of age. It is very much influenced by the geographical environ- 
ment, being more common in districts exposed to the southwest wind, 
and above glacial clay than above glacial sand, and is less common 
in those districts in which there is a larger number of deaths from 
tuberculosis in children, where there is a high mortality from phthisis 
in “middle age,’ and in places where there is a considerable amount 
of tuberculous milk. Persons exposed to wind and wet, as seamen, 
dock laborers, agriculturists, etc., are more liable to succumb to this 
type of phthisis. It appears from Brownlee’s statistics that the inci- 
dence of this type has no relation to the hygienic surroundings, or with 
overcrowding of population; it is associated rather with rural than 
with urban conditions. 

The Middle Age Type——The second type of phthisis has its incidence 
in middle age, killing most commonly between forty-five and fifty 
years. It is independent of the geographical and meteorological 
environment, of wind, and the nature of the subsoil, and is more 
common in those districts in which there is a large number of deaths 
from tuberculosis in children, and a large amount of tuberculous milk. 
It is especially common in persons pursuing certain occupations, 
mainly those associated with dust and silica. This type of phthisis 
is greatly influenced by hygienic conditions and density of population. 
Brownlee interprets these facts as follows: 

“(a) Many persons infected with tuberculosis in childhood seem, 
after obtaining some degree of immunity, to go through life compara- 
tively well, the organism of tubercle, however, remaining living though 
in a quiescent stage. As the strain of life increases, and the resistance 
falls, this chronic process seems, in a considerable number of cases, 
to flare up into an acute process, which results in subsequent death. 
This, however, would probably not account for more than two-fifths 
of the cases. 

“(b) It is to be noted that the age at which middle-age persons die 
of tubercle is the same at which insanitary conditions have been shown 
to produce the most depressing effects, namely, between the ages of 
forty and fifty. Infection in middle-age would also seem to be common, 
especially among workers in silica.”’ 

The Old Age Type.—This type occurs mostly among persons fifty-five 
and sixty-five years of age, is especially common among miners of 
coal, lead, iron, ete., and among workers in slate quarries. It appears 
to be independent of hygienic conditions or the density of population, 
and no external factor has been found associated with it. 

Brownlee attempts to offer two possible explanations for these 





100 THE EPIDEMIOLOGY OF TUBERCULOSIS 


epidemiological peculiarities of phthisis. The first is that there are 
two distinct strains of the bacillus of tuberculosis. These different 
strains have each a special age distribution. One of the strains attacks 
in early manhood and possibly also in old age, the other in childhood 
and middle life. The one is associated with the country, and the other 
with the town. The second explanation offered is that the physiological 
response to attack by the organism may be different, according to 
the environment in which the individuals attacked have lived. From 
the first hypothesis it would appear that each type of organism confers 
a certain degree of protection against the other. An analogy is to be 
seen in the two distinct types of smallpox observed in England and 
attributed to distinct types of organisms; the same is apparently true 
of typhoid and paratyphoid. The second hypothesis is in agreement 
with the almost universal observation that mild infection with tubercu- 
losis establishes some degree of immunity to the disease in those who 
survive. The result is that when the young adult stage of life is reached, 
the disease is absent. If, on the other hand, no immunity has been 
established when infection took place, the disease is often fulminant. 
Later, when the strain of life in cities begins to tell, namely, between 
forty and fifty years, those persons at the ages where the strain is most 
felt, tend to succumb. In the country the health of persons at these 
ages is good, and consequently death from phthisis at this age is rare. 

The conclusions of Brownlee have great epidemiological bearings, 
and prophylactic measures, to be proved effective, must evidently be 
judged by their effect on the different types of the disease. The subject 
deserves further study in other countries. 


CHAPTER IV. 
PHTHISIOGENKESIS. I. 


PREDISPOSITION, ENDOGENOUS AND EXOGENOUS. 


Tue data presented in the preceding chapters have shown con- 
vineingly that tuberculosis is a transmissible disease, caused by the 
entry of the tubercle bacilli into the body. But it was also made clear 
that while no tuberculosis can occur without tubercle bacilli, infection 
with the germs is not invariably followed by that train of symptoms 
which we know as tuberculous disease. Indeed, forty years of intensive 
study of the bacteriology of tuberculosis has demonstrated that only in a 
relatively small proportion of cases is infection followed by tuberculous 
disease; the majority of human beings bear this infection without any 
harm. On this point nearly all authorities agree. As was already men- 
tioned, the only difference of opinion among pathologists at present 
is whether as many as 95 per cent of civilized humanity show evidences 
that tubercle bacilli have been implanted in the tissues of their bodies, 
or merely 70 per cent. Just as the presence of meningococci in the 
rhinopharynx does not invariably produce meningitis, pneumococci, 
pneumonia, Pfeiffer’s bacillus, influenza, ete., so do not tubercle bacilli 
produce tuberculous disease in all cases in which they have gained an 
entrance into some vital tissues, even though they may have succeeded 
in producing gross or microscopic changes in the structure of the 
organs. 

Constitutional and Environmental Causes.—Succeeding in elucidat- 
ing tuberculous infection, but failing to explain satisfactorily tubercu- 
lous disease, bacteriology is at present considered by many authors 
as incapable of clearing up completely the etiological problems of 
phthisis. This is not only true of tuberculosis but of nearly all other 
infectious diseases. ‘Today we know that to have identified the 
microbic agent of any pathological process,” says Theobald Smith,! 
“is but the beginning of the solution of the immediate problem and 
that it answers but one of a long series of questions.’’ During recent 
years thoughtful minds in the medical world have therefore again 
directed their attention to other factors, endogenous and exogenous, 
which are instrumental in the production of pathological processes. 
The problems of heredity and environment, susceptibility, predisposi- 
tion, and immunity are studied a'ong new lines of research. Attempts 
are being made to unravel the mystery why when several persons are 


1 Science, 1921, N. S., 54, 99. 


102 PHTHISIOGENESIS 


exposed to infection with tubercle bacilli, and infected, some may 
become sick, while most remain in comparative, or complete, health; 
why in familial tuberculosis, a few descendants of phthisical parents 
will develop tuberculous disease and perhaps die as a result of it, 
while several others equally exposed to infection remain healthy; 
why of those who become sick, some, though very few, suffer from a 
very acute and rapidly fatal disease, like miliary tuberculosis, or pneu- 
monic phthisis, while many others have a chronic, but progressive 
disease, like pulmonary tuberculosis of the common type; why in still 
others, the virus produces evident changes in the lungs and pleura, 
but the process is abortive, the patient and his physician knowing 
little, or nothing of the infection. Reasons are sought for the prefer- 
ence of the virus to attack in some people the lungs, in others the glands, 
joints, bones, or serous membranes of the chest, abdomen, or the cere- 
brospinal axis. We are seeking light on the problem why clinical mani- 
festations of tuberculous infection are observed only in a small propor- 
tion of individuals who harbor tubercle bacilli, while the vast majority 
in whom we know that the virus has undoubtedly been implanted in 
the tissues, produces anatomical changes in structure, unmistakably 
recognized at the necropsy, yet these lesions healed spontaneously 
without producing any obvious symptoms. 

Various explanations have been given for these obvious differences 
in the pathogenesis of tuberculosis. Some have maintained that the 
variability of morbid phenomena is due to differences in the type and 
the virulence of the tubercle bacilli. But we have already shown that 
nearly all the tuberculous disease in adults is due to the human type 
of bacillus, and so is extrathoracic tubercle in children. It is also agreed 
that a study of the virulence of various strains of the virus isolated 
from the many clinical forms of the disease sheds no light on the 
problem. Guinea-pigs, monkeys, and primitive human beings, when 
exposed to infection, and infected, almost always suffer from the acute 
forms of the disease. Civilized human beings, infected spontaneously, 
mostly suffer from the chronic forms of phthisis, and in the vast 
majority of cases tuberculous infection is but an adaptation of the 
parasite to the host, both of which live in symbiotic relationship with 
each other. 

Attention has recently been turned to accessory non-parasitic causes 
of phthisis, among which there are many, including endogenous, such 
as heredity, anatomical and biochemical peculiarities of the individual, 
etc., and also exogenous, including environmental peculiarities, such as 
economic conditions including occupation, housing, nourishment, ete., 
and also the geographical milieu. As will be seen from the succeeding 
pages, the results have so far been very meagre, but when a bacteriolo- 
gist of the magnitude of Theobald Smith is constrained to say that 
non-parasitic factors are necessary conditions in the origin of infectious 
diseases, and far outweigh the living agent in etiological significance, 
it is clear that they are worthy of intensive study. 


HEREDITY 103 


HEREDITY. 


Statistical Study.— lor centuries it has been noted that in certain 
families tuberculosis reappears in successive generations; many tuber- 
culous patients can trace the disease back to their ancestors and blood 
relatives. Statistics collected along these lines are plentifully avail- 
able in medical literature, but on close analysis it appears that they are 
of little value in proving or disproving the hereditary transmission 
of the disease, or a predisposition to it. 

The element of contact with “carriers,’’ or sources of infection, is 
always disturbing. Moreover, the ubiquity of the disease, one out of 
every seven or eight deaths is due to tuberculosis, so that it may be 
found in every large family or its collaterals, would lead us to expect 
that most tuberculous patients may find some relative who has had 
the disease. Then it must be mentioned that facts pertaining to 
heredity are derived from statements of patients in answer to leading 
questions, and these are open to criticism. Even questions about their 
personal history are not accurately answered, as a rule. Our patients 
at the Montefiore Hospital nearly always state that they had measles 
during childhood, probably on the principle that everyone must have 
it. But very few say that they have had diphtheria, typhoid fever, 
typhus, scarlet, etc., although most of them come from Eastern Europe 
where these diseases are rampant, and hardly any attempt worth men- 
tioning is made to check them by proper quarantine regulations, and 
very few indeed escape. Very few know the real cause of death of their 
parents; in fact, it would seem as if their parents were all immune to 
tuberculosis, considering that the patients do not mention it after 
questions are addressed to them on the subject. 

In private practice, where we deal with a more intelligent class, 
we often find that the father is stated to have coughed, the mother 
had hemoptysis, ete., after a categorical answer that there has been 
no consumption in the family. On the other hand, we know how much 
suggestion, through leading questions suitable for a certain purpose, 
may bring out appropriate answers. Many patients are convinced 
that their blood is not by any means “tainted,” that they “come from 
healthy stock,” that “there has never been any consumption in the 
family,” etc. Moreover, the few facts obtained from patients, intelli- 
gent and otherwise, refer to the incidence of pulmonary tuberculosis, 
while extrathoracic tuberculous lesions in parents, brothers, and sisters, 
are almost always forgotten; at any rate not mentioned. As a rule, 
only fatal cases are mentioned, while those who have had the disease 
but recovered, are forgotten. 

Statistical proof of the hereditary transmission of tuberculosis, or 
a predisposition to it, will only be satisfactory: when careful records 
of many patients are kept for several generations in which children 
of tuberculous parentage have succumbed to the disease despite 
the fact that they have been removed immediately after birth, thus 


104 PHTHISIOGENESIS 


preventing exposure to infection through intimate contact. To be 
of scientific value, they should be based on detailed postmortem 
examinations of the parents and grandparents, and even of collaterals. 
Such data we do not have. The frequently cited statistics obtained in 
orphan asylums showing that thousands of children of tuberculous 
parentage failed to develop tuberculosis, are absolutely of no value 
in disproving either heredity, or infection of this disease. In these 
institutions children under fourteen years are usually kept, and at 
that age active pulmonary phthisis is exceedingly rare, as has already 
been shown. 

For these reasons very little confidence can be placed in the statis- 
tical compilations of various authors to the effect that among their 
patients 25, 44.7, or 59.2 per cent have given a history of tubercu- 
losis in the parents, grandparents, brothers, sisters, or collaterals. 
It depends a great deal on the zeal of the questioner to obtain points 
for the substantiation of his pet theory. Even the excellent statistical 
studies of Karl Pearson, Weinberg, Schliitter, and many others, are 
not at all convincing. In fact, Burckhardt! found that in non-tuber- 
culous persons, tuberculosis in the ascendency is just as strongly 
represented as in the tuberculous, and that the disease in the father 
is just as frequent in both groups, while the frequent occurrence in 
the mothers, fathers, brothers, sisters, uncles, and aunts, can be easily 
explained by infection. 

Raymond Pearl? has recently attempted to meet the various objec- 
tions to the statistical data thus far published by an ingenious method. 
He argues that if heredity is a factor of importance in the etiology 
of clinically active tuberculosis it would be reasonable to expect that 
a tuberculous individual would have a larger proportion of tuberculous 
among his or her blood relatives, both direct and collateral, and in 
ascending and descending generations from the individual, than would 
a person who was not tuberculous. His study is based on data obtained 
from 57 family histories, involving over 5000 blood relatives. Of 
these 38 were tuberculous, and 19 nontuberculous. Though the number 
of families is small, they may be regarded as random samples of the 
working population of Baltimore. His results showed that taking all 
generations together, it appears that a tuberculous person has 7 per 
cent of his or her blood relatives tuberculous, whereas a nontubercu- 
lous person, chosen at random, has only 1.2 per cent of his or her rela- 
tives tuberculous, and the absolute number involved in the two samples 
being absolutely the same. In other words, tuberculous persons have 
nearly six times as many blood relatives tuberculous as have non- 
tuberculous. But closer analysis of his data led Pearl to the conclusion 
that familial contact with active open cases is beyond question a factor 
in determining the incidence rate of clinically active tuberculosis. 

It is thus clear that the statistical method thus far has neither 


1 Ztschr. f. Tuberkul., 1904, 5, 29. 
2 Am. Rev. Tubercul., 1920, 4, 688. 


BIOLOGICAL ASPECTS OF TUBERCULOUS HEREDITY 105 


proved nor disproved the hereditary transmission of the disease. 
Moreover, “if we allow that 50 per cent of the offspring of those suffer- 
ing from pulmonary tuberculosis eventually suffer from this form of 
the disease, owing to their inherited want of resistance we should, I 
think, expect a progressive increase in the total mortality provided we 
bear in mind the increase of population. But the reverse appears to 
be true” (Latham). On the other hand, the most learned apostle 
of the theory of heredity of tuberculosis, Karl Pearson,! has this to say: 
“We do not suppose tuberculosis to be handed down from parent to 
offspring any more than we should suggest that the wearing of spec- 
tacles is hereditary. We merely suppose that certain constitutions 
are more and certain other constitutions are less resistant to, say, 
pulmonary tuberculosis. It is immaterial whether the tuberculous 
diathesis is looked upon as an inheritance of susceptibility or an inheri- 
tance of resistance, for both are but grades in the scale of immunity 
peculiar to the individual. In a community wherein tuberculosis has 
been prevalent for many centuries we should anticipate that natural 
selection would steadily intensify their immunity by eliminating those 
with less resistance; the higher grades of resistance survive and are 
transmitted by heredity. In a community wherein the tubercle bacillus 
has not been introduced there will have been no selection to raise the 
average degree of immunity; there will, however, be many grades of 
susceptibility, and those will be inherited, whether or not they have 
been put to the test of an infected environment.’ Our study of the 
epidemiology of tuberculosis (Chapter III) has brought forth evidence 
in favor of this view. 


BIOLOGICAL ASPECTS OF TUBERCULOUS HEREDITY. 


The reappearance of tuberculous disease in several successive 
generations is by no means conclusive proof that the disease, or that 
a predisposition to it, has been transmitted by heredity. We find in 
coal miners anthracotic changes in the lungs through several genera- 
tions; so long as they are engaged at that occupation. But no geneticist 
will agree that we deal here with biological heredity. Likewise, the 
social, economic, hygienic, and sanitary conditions and surroundings 
which were responsible for phthisical disease in the parents may be, 
and usually are, operative in the children who remain in the same 
social milieu. In these cases sociologists speak of social heredity; it 
is not a biological phenomenon. Biological heredity implies the trans- 
mission of characters, or their physical foundations, which were con- 
tained in the germ plasm, or the parental sex cells, at the moment of 
fertilization. Anything that may have affected the fertilized ovum, 
or the embryo, cannot be considered inherited, because intra-uterine 
infection, and germinative transmission of a disease, have nothing 


1 Lancet, 1920, 2, 891. 


106 PHTHISIOGENESIS 


to do with the problems of heredity, just as extra-uterine influences 
cannot be considered transmissible in the biological sense. 

As physicians, engaged in the study and prevention of the disease 
we must consider possibilities of embryonic infection, irrespective of 
its relation to the problems of heredity in the strict biological sense. 

1. The unfertilized ovum may be infected from the mother. 

2. The semen or the spermatozoa, infected from the father, may 
bring along the virus when reaching the ovum. 

3. Tubercle bacilli may infect the fertilized ovum. 

4. The embryo may be infected by bacilli in the mother’s blood. 

{xperimental investigations by Friedmann show that intra-uterine 
infection with tubercle bacilli is not impossible. This, to some degree, 
confirms Baumgarten’s theory to the effect that tubercle bacilli may 
enter the blood stream of the fetus, remain dormant for a long’ period 
of years, to flare up again by intense multiplication when, for some 
reason, the natural resistance of the body fails. This form of trans- 
mission of phthisis cannot be considered germinative heredity in the 
strict sense of the word—it is actually infection of the fetus from the 
mother—yet it is important for the clinician, especially to one giving 
thought to prophylaxis, and the modern teachings of eugenics. 

Baumgarten! based his theory mainly on experiments with tuber- 
culous birds. It is well known that the progeny of tuberculous chickens 
is tuberculous even under conditions in which infection after the egg 
has been laid can be positively excluded. It has been demonstrated 
experimentally that the albumen of a fertilized egg may be inoculated 
with tubercle bacilli, and the evolution of the chick goes on as may 
be expected; but it develops tuberculosis after it is hatched. This 
has been observed by Baumgarten, Milchner, Girtner, Maffucci, 
Koch, and others. Intraovular infection has also been observed in 
cattle, and it shows that infection of the ovum, after fertilization, does 
not invariably destroy it. It may keep on growing and evolve into a 
living organism, even though it develops tuberculous disease soon after 
birth. In human beings, there have been found instances in which 
localized, calcareous changes of some focus in the lungs were seen in 
newborn infants, showing that they had tuberculous disease in utero 
and that the lesions had healed. 

Spermatogenic Infection.— We are in the dark as to how the bacilli 
reached the embryo in such cases. Some authors maintain that the 
semen may be infected, and the bacilli are carried by the sperma- 
tozoa. Spano, Porter, Friedmann, and others have, in fact, found 
tubercle bacilli in the semen of persons who died from acute miliary 
tuberculosis, and such as have suffered from tuberculous disease of 
the generative organs. It is important to bear in mind that persons 
with tuberculous disease of the testicles, seminal vesicles, prostate, etc., 
at times cohabit with the opposite sex, and pregnancy occurs quite 


1 Arb. a. d. Gebiet d. pathol. Anatomie u. Bakteriol., 1891-1892, vol. 1; Lehrbuch d. 
pathogenen Mikroérganismen, Leipzig, 1911, p. 710. 


BIOLOGICAL ASPECTS OF TUBERCULOUS HEREDITY 107 


often in such cases. Indeed, Albrecht, Cavagnis, Maffucci, and others, 
have succeeded in infecting rabbits and guinea-pigs, with semen taken 
from bulls suffering from tuberculosis. Friedmann! injected an emul- 
sion of tubercle bacilli into the vagina of rabbits immediately after 
they had been impregnated by the males. Subsequent observation 
showed that while the mothers remained free from disease, tubercle 
bacilli were found in sparing numbers in the seven-day-old fetuses, 
which were apparently not at all hampered in their evolution. In 
the newborn rabbits, whose mothers were thus treated, tubercle bacilli 
were found in various organs. These findings were taken as evidence 
to the effect that spermatogenic infection, 2. e., infection with tubercle 
bacilli brought along with the semen from a tuberculous father, is 
possible. 

It appears, however, that things are not so simple. Semen con- 
tains tubercle bacilli only when the generative organs, especially the 
testicles and seminal vesicles, are affected by tuberculous disease, 
though Jani, Spano, Jackh, Nakarai, and Simmonds have found 
numerous tubercle bacilli in the apparently normal seminal vesicles 
of patients suffering from tuberculosis of the lungs. Rational con- 
sideration, however, leads one to the suspicion that all this is not 
sufficient proof that spermatozoa, or the ovum, are infected with 
tubercle bacilli. The size of the mammalian ovum and spermatozoén 
renders it extremely improbable that they should become infected 
with these germs. Indeed, it may be stated that no one has ever seen 
a spermatozo6n, or an ovum, in which a tubercle bacillus could be 
discerned under the microscope. Moreover, if they were infected, 
they surely could not go on developing; even if they were not killed, 
they would undoubtedly be rendered sterile. The fact that semen is 
occasionally found to contain tubercle bacilli, as is shown by its 
potentiality to infect animals, does not prove that germinative infec- 
tion ever takes place. Clinically we see very frequently that children 
begotten by tuberculous fathers, even those who have tuberculous 
lesions of the generative organs, are well developed; on the average, 
as well as those of apparently healthy parentage. Moreover, we know 
of no case reported in which a father with tuberculosis of the testicles, 
seminal vesicles, or prostate, had begotten a congenitally tuberculous 
infant, though Hildebrand reports a series of cases in which intercourse 
with men having tuberculous testicles was responsible for tuberculous 
disease of the female generative organs. Even conceding that the 
tubercle bacilli may implant themselves on spermatozoa, and then, 
at the time of fertilization, infect the ovum, it must be an exceedingly 
rare occurrence. We must recall that with each emission over twenty 
millions of spermatozoa are expelled, and that the one on which a 
tubercle bacilli has implanted itself should be just the one that fer- 
tilizes the ovum, is a rather remote chance. This mode of infection 


1 Ztschr. f. klin. Med., 1901, 58, 2. 


108 PHTHISIOGENESIS 


of the ovum may thus be left out of consideration when speaking of 
tuberculous heredity. 

Placental Transmission.— Many diseases are often transmitted from 
the mother during pregnancy; smallpox, syphilis, leprosy, ete., are 
good examples of intra-uterine infection of the healthy fetus from a 
sick mother. That the placenta may harbor tubercle bacilli is well 
known; the frequent bacteriemia in phthisis explains it. Lehmann, 
Runge, Nowack, Auche, Chamberland, Warthin, Weller, and many 
others, have found tubercle bacilli in the human placenta. On care- 
fully examining the histology of the placenta of phthisical pregnant 
women Schmorl and Geipe! found tubercle bacilli in 9 out of 20 cases. 
One of the 9 women had merely an incipient apical lesion. Schmorl 
estimates that 50 per cent of pregnant phthisical women have tubercle 
bacilli in their placentas. He maintains that tubercle bacilli may enter 
the placenta during any period of pregnancy, and in any stage of the 
disease, but that they are mostly found in the advanced stages of 
phthisis, and in acute miliary tuberculosis. The fetus may be infected 
from the mother during the act of birth, when vigorous contractions 
of the uterus may lacerate some of the less resisting parts of the 
placenta. But there is a possibility of earlier infection. It is, to be 
sure, only a remote possibility that the virus should directly enter 
the fetus, if it is at all possible, but it may be brought along with blood 
through the umbilical vein; or by way of the intestine after it reached 
the amniotic fluid and is then swallowed, or aspirated by the fetus. 
According to Andrews, Heller, Sitzenfrey, Rietschel, Ghon, and others, 
the amniotic fluid at times contains tubercle bacilli. In some cases 
they may infect the chorion and, by extension, tuberculosis of the 
amnion may result, the bacilli passing into the amniotic fluid. The 
fetus, by aspiration of the fluid, is thus infected with resulting primary 
tuberculosis of the lungs. Such cases may be considered bronchogenous 
infection. However, of the cases of intra-uterine infection reported, 
none survived a year. Nearly all succumbed within a few weeks. 
Most were stillborn. 

However, while all this is possible, it appears to be a rare phenome- 
non. According to Lowenstein? only about 30 authentic cases of tuber- 
culosis of the placenta have been reported in the literature. 

Congenital Tuberculosis.—The rarity of intra-uterine infection is 
also evident when we bear in mind that cases of congenital tuberculosis 
are comparatively rare. It has been repeatedly stated that it is very 
frequent in cattle. But, according to Lubarsch,’ there have altogether 
been reported only 230 cases of congenital tuberculosis in calves under 
three days of age, of which 215 may be considered as due to placental 
transmission. In humans it appears even more rarely, and of those 
reported, only a small proportion can be considered real instances of 


1 Ziegker’s Beitr., 9, 428; Miinchen. med. Wehnschr., 1904, p. 1576. 
2 Vorlesungen tiber Tuberkulose, Jena, 1920, p. 175. 
3’ Ztschr. f. Aerztliche Fortbildung, 1918, 15, 144. 


BIOLOGICAL ASPECTS OF TUBERCULOUS HEREDITY 109 


congenital tuberculous disease. The first undoubted human case was 
reported by Schmorl and Birch-Hirschfeld.!| The mother died from 
acute general miliary tuberculosis in the seventh month of pregnancy. 
The placenta appeared normal macroscopically, but microscopically 
tuberculous changes were found, and tubercle bacilli were demon- 
strated in the blood from the umbilical vein. Apparently the mother 
infected the fetus shortly before death. Londe? was the first to inves- 
tigate the offspring of tuberculous mothers by inoculation tests, and 
he obtained positive results in some cases—guinea-pigs were infected 
when inoculated with the placental tissue, the fetal blood, and other 
organs. The placenta was found the most virulent tissue. Warthin 
and Cowie? reported several cases in this country, but even they warn 
that “intra-uterine transmission of tuberculosis is possible, but 
extremely rare, and needs to be supported by further research before 
it can be taken as final.”” Martha Wollstein‘ described a case in which 
the mother died six days after confinement, and the child died nineteen 
days after birth. The placenta showed advanced tuberculous changes, 
and the infant showed miliary tuberculosis of the lungs, spleen, kidneys, 
and mesentery. It is, however, noteworthy that tuberculosis of the 
placenta, which is more common, may not affect the fetus. Thus, 
A.S. Warthin’ and Carl Vernon Weller® have reported cases of placental 
tuberculosis, and still the infants thrived for months after delivery.? 

Another point is that it is rare that tuberculous changes should be 
found macroscopically in newborn tuberculous infants in whom tubercle 
bacilli are demonstrated microscopically and by inoculation tests. 
This form of congenital tuberculosis has been named by Honl Status 
bacillaris with a view of distinguishing it from true congenital tubercu- 
losis with structural changes of a tuberculous nature; in the former, 
no macroscopic nor microscopic changes are found; while in the latter 
they are found, though both are capable of infecting when the tissues 
are injected into animals. 

Of the cases which have been reported as congenital tuberculosis, 
very few are accepted as such by careful critics. In most, it has been 
shown the evidence is against their being really instances in which 
intra-uterine infection took place. Thus Péhu and Chalier’ found only 
51 authentic cases on record in medical literature. It may be added 
that most of the cases were not conclusively proved. Rémer*® knows of 
but 30 cases, and some of them may be said to be reliable only “in 
all probabilities.” Péhu and Chalier believe that in these cases infec- 
tion usually takes place at the end of pregnancy when the placental 


1 Ziegler’s Beitr., 1891, 9, 428. 2 Rev. de la tuberculose, 1893, 1, 125. 

8 Jour. Infect. Dis., 1904, 1, 140; Ibid., 4, 347. 

4 Arch. Pediat., 1905, 22, 321. 

5 Arch. Intern. Med., 1916, 17, 509. 6 Jour. Am. Med. Assn., 1913, 61, 1951. 

7 A good review of the literature of congenital tuberculosis may be found in F. Parkes- 
Weber’s paper in the British Jour. Children’s Dis., 1916, 18, pp. 321 and 359. 

8 Arch, de méd. des enfants, 1914, 17, 721, 9 Log, cit., p. 276, 


110 PHTHISIOGENESIS 


circulation is established and results from a bacteremia which is usually 
a terminal event. They should therefore be regarded as examples of 
transplacental heredocontagion, and not of direct heredity. 

It is thus shown that, theoretically, placental transmission of tuber- 
culosis is possible. But available facts combine to prove that it is 
exceedingly rare among human beings. Indeed, when compared with 
the enormous number of infections after birth, the few recorded instances 
of congenital tuberculosis sink into insignificance. After all, when it does 
occur at all, it is from mothers who are in the far-advanced stages of 
phthisis, or who have tuberculous disease of the genito-urinary system. 
Such women conceive only rarely. It is a fact worthy of note in this 
connection that numerous examinations of stillborn fetuses from 
phthisical mothers have not revealed any traces of tuberculous infec- 
tion; even inoculation experiments have failed in most cases. 

Among cattle congenital tuberculosis appears to be more frequent 
than among humans. Still, the application of the well-known Bang 
system has shown that, even here, it is exceedingly rare. In the United 
States, Harlow Brooks! has shown that when calves are removed from 
their tuberculous mothers immediately after birth, they do not develop 
the disease. 

Handicap of the First-born.—Among the various constitutional 
and congenital factors in the etiology of tuberculosis there is also to 
be mentioned that the first-born in a family is most likely to develop 
the disease. As is well known, in many countries the first-born has 
certain prerogatives, especially among the so-called noble classes. 
But statistical evidence gathered by geneticists tends to show that 
their vitality is of inferior quality when compared with those who 
succeeded in the order of birth: They weigh less, are more frequently 
stillborn, abortions being more frequent among newly married women, 
and of those who come into the world alive a much larger proportion 
succumb during the first year of life than of the later-born children. 
Karl Pearson,? Séren Hansen,’ and others have shown statistically 
that inferior physique, feeble-mindedness, epilepsy, and especially 
tuberculosis are more likely to occur in first-born, then in the second- 
and third-born, and least in those who are the fifth, sixth, ete., in a 
family. 

Pearson showed that whereas the average incidence of tuberculosis 
would be 67 if the patient’s number in the family was of no etiological 
moment, the actual incidence for the first-born was 113; among the 
second-born the ratio of the actual to the expected being 79 to 64. In 
a study of 3522 tuberculous patients at Copenhagen, Hansen found 
that there were 386, or about 64 per cent more first-born than there 
should be if the birth number was of no consequence. Among 2113 
patients from the Boserup Sanatorium he found that the second- and 


1 Am. Jour. Med. Sci., 1914, 147, 718; Tr. Soc. Exper. Med. and Biol., 1914, 11, 50. 
2 A First Study of the Statistics of Pulmonary Tuberculosis, London, 1907. 
3’ Eugenics Review, 1913, 5, 252. 


CLINICAL ASPECTS OF HEREDITY nit 


third-born are also more liable to develop phthisis, as can be seen from 
the following table: 


Number Men. Women, 

in family. Calculated. Actual. Calculated. Actual. 
[Aen a. Shy. ena, aia as ite O28, 551 274 437 
Zac ee: 5 Ae “ee aa aol 389 261 324 
Dee. eke te oR ae eee 313 238 255 


It may be suggested that the first-born of tuberculous parentage 
being older, have been exposed to the risks of infection for a longer 
time and they thus swell the number of tuberculous patients. But 
H. Kjerrulf found among school children the number giving positive 
skin reactions to tuberculin is not larger among the first-born than 
among the later-born. 

Those interested in problems of eugenics point to the fact that, 
inasmuch as the tendencies to small families have of late become very 
pronounced in certain countries, the inferior stamina of the first-born 
are bound to become of greater danger as regards the prevalence of 
tuberculosis and other physical and mental defects. However, it 
appears that while in France, because of the low birth-rate, the propor- 
tion of first-born is larger than in other countries, the tuberculosis 
mortality is very high, this does not hold for other countries. It is 
clear that the tuberculosis mortality has been declining with the decline 
in the birth-rates in nearly all civilized countries. In countries with 
exceedingly high birth-rates, like Russia, Hungary, etc., the mortality 
from this disease has been extremely high. 

Clinical Aspects of Heredity.— Many authors have observed certain 
clinical phenomena which cannot be explained otherwise than by 
heredity, either of the disease, or of a predisposition to it. Brehmer, 
and after him several other writers, found that in many cases the 
onset of the disease occurs at the same age in parents and children. 
Piéry found that in many families the children mostly succumb before 
attaining the age of sixteen. While many cases can be cited in sub- 
stantiation of these observations, it appears that, so far, a sufficient 
number have not been collated to prove their significance conclusively. 
The familial occurrence of the disease can be explained by infection 
just as by hereditary transmission, as has already been stated. 

Of greater moment is the inheritance of the locus minoris resistenti@, 
which Brehmer described long ago, and Turban,! Baldwin,? Moller, 
Kuthy,’ and others have confirmed it. It appears that when pulmonary 
tuberculosis occurs in parents and children, the chances are immense 
that the same side of the chest should be affected in each case. This 
family resemblance in phthisis has been found in about 75 per cent of 
cases. In my own experience I also observed that in about two-thirds 
of cases the side affected was the same in the several affected members 


1 Ztschr. f. Tuberk., 1900, 1, 30. 2? Yale Med, Jour., 1902, p. 215, 
8’ Ztsehr. f. Tuberk., 1913, 20, 38, 


112 PHTHISIOGENESIS 


of the family. Moller’ points out that when a child suffers from a 
tuberculous lesion of some bone, the chances are that when its brother 
or sister develops tuberculosis it will also be a disease of bone, and 
not of the soft tissues. These facts are explained by the assumption 
that some organs or tissues in the body lack powers of resistance, and 
that this defect is transmitted by heredity. This will be discussed 
again when speaking of the thoracic anomalies and their relation to 
phthisiogenesis. Meanwhile it may be stated that these problems 
have not received the careful study they deserve. 

Disturbances in the Metabolism as Predisposing Factors.—In the 
search for the factors predisposing to phthisis many have looked into 
the metabolism of the body, stating that tuberculous infection is 
harmless in the vast majority of persons, so long as the metabolic 
processes are normal; only when certain disturbances occur in this 
regard can phthisis develop. It is, however, a fact that in the enor- 
mous literature on the subject of tuberculosis, we cannot find an 
exhaustive study of the metabolism of persons affected with the disease, 
and hardly anything about the metabolism in the so-called pretuber- 
culous stage. 

Several authors have maintained that an excessive excretion of cal- 
cium in the urine can be found in all cases of phthisis long before the 
onset of the disease. In this country, Croftan,? John F. Russell, and, 
more recently, John O. Halverson, Henry Kk. Mohler and Olaf Ber- 
geim® have made some studies along these lines. The last-named 
investigators have found that the calcium content of the blood of 
patients with advancing and convalescing tuberculosis revealed that 
in incipient cases in which the patients, who were on a high milk diet, 
showed marked improvement, the values for calcium in the serum were 
normal and fairly constant. In advanced cases the variations obtained 
were greater (some rather high and some rather low values being 
obtained), and improving patients showed on the average slightly 
higher values than the unimproved. No marked deviations from the 
normal, however, were observed in the calcium content of the serum 
of patients in various stages of pulmonary tuberculosis. It is the 
opinion of these investigators that the failure of the body to deposit 
lime around the tuberculous areas is to be ascribed not to a deficiency 
in blood calcium, but rather to an inability of the cells of the tubercu- 
lous area to utilize available calcium. 

Several French savants, notably Robin, Binet, etc., have found that 
in the pretuberculous stage there is a pronounced excess in the excre- 
tion of inorganic salts in the urine, notably those of lime and magnesia. 
The result is that the blood, bones, and lung tissues show a distinct 
lack in these mineral salts. Gaube found that the descendants of 
phthisical subjects excrete on the average more calcium and magnesia 


1 Lehrbuch d. Lungentuberkulose, Berlin, 1910, p. 30, 
2 Sixth Intern. Cong. Tubere., 1908, 1, 275. 
3 Jour. Am. Med. Assn., 1917, 68, 1309, 


ENDOCRINE DISTURBANCES 113 


than those of healthy stock. Robin sees in this lime and magnesia 
starvation an excessive amount of self-combustion, and he considers 
this anomaly in the metabolism the main element in the preparation 
of the soil prone to tuberculosis, whatever the remote cause may be— 
heredity, alcoholism, malnutrition, overwork, etc. Infection alone is 
insufficient to produce phthisis, as is evident from the fact that most 
people infected with tubercle bacilli escape the disease. It is only 
when the soil is prepared by the dissimilation and emaciation, by 
pretuberculous decay, as Robin calls it, that phthisis may develop. 
The gravity of the pulmonary lesion goes hand-in-hand with the 
degree of lime starvation, demineralization and emaciation of the 
body. According to these writers, phthisis is preventable. Demine- 
ralization of the body must be sought and, when discovered, prevented 
by the administration of remedies tending to replace the lime and 
magnesium which are being eliminated from the body excessively. 

These and other findings about the metabolism in phthisis have 
not been confirmed by all who have made careful studies along these 
lines. It appears that in the vast majority of consumptives the metabo- 
lism is quite normal so long as there is no high fever. The occasional 
lapses in the metabolism are explained by the usual causes of morbid 
phenomena observed in other diseases characterized by fever, emacia- 
tion, debility, etc. This has been confirmed by the studies of McCann 
and Barr,! who found that the basal metabolism of tuberculous patients 
may be normal or slightly above that of normal men of the same size. 
With the increase in the temperature there may occur an increase in 
the basal metabolism, but it is not large. The basal heat production 
in tuberculosis may be less than the normal for the same patient in 
health. In other words, the loss in weight may be accompanied by 
a reduction in metabolism which more than compensates for the ten- 
dency to increase caused by the disease. However, the basal metabo- 
lism in the pretuberculous stage, 7. e., in those in whom tuberculosis 
has not yet been developed fully in the clinical sense, has not been 
studied as yet. We do not know whether any changes in this direction 
predisposes to the evolution of tuberculous disease. At any rate, this 
subject has not been studied sufficiently to permit making generaliza- 
tions. 

Endocrine Disturbances.— Recent studies of endocrine disfunctions 
have shown that changes in the structure and functions of the internal 
secretory glands are very frequently encountered in tuberculous 
patients, though hardly any etiological relationship has been estab- 
lished. Considering that tuberculosis is so widely prevalent, it is to 
be expected that some should present evidence of glandular disturb- 
ances. However, it appears that certain glandular conditions favor 
the development of tuberculous disease, while others prevent it more 
or less. While studies on the etiological relationship of the endocrines 


1 Arch. Intern. Med., 1920, 26, 663. 


114 PHTHISIOGENESIS 


to tuberculous disease have not been as thorough and as abundant as 
appears desirable, still some facts are already available which are 
very suggestive. 7 

As will be shown later on (see Chapter XXX), excessive secretion 
of the thyroid gland protects, in a measure, against the development 
of active and progressive tuberculosis. It appears that hyperthyroid 
individuals only rarely suffer from active phthisis, and when symptoms 
of this disease present themselves, the pulmonary lesion is mild, and 
manifests strong tendencies to cicatrization. This clinical fact was 
already noted by Hamburger as far back as 1853, and in 1887 S. Solis 
Cohen pointed out that a large thyroid is characteristic of immune 
members of tuberculous families. Morin! observed that in familial 
thyroid disease, the members of the family that had large thyroids 
with hyperfunction of the gland did not develop tuberculosis, while 
25 per cent of 348 cases with atrophy of the thyroid became tubercu- 
lous. “Atrophy, or defective development of the thyroid,” says 
Sajous,? “is commonly observed in persons predisposed to tubercu- 
losis and other infections. Indeed, the prominence of Adam’s apple 
in such subjects is due to the fact that a flat thyroid fails to fill suffi- 
ciently the infrathyroid portion of the neck to preserve its normal 
shape. (Emaciation, however, has a great deal to do with it.) Such 
a diminutive thyroid may be due to deficient antenatal or postnatal 
development, but in many instances it is traceable to infectious 
disease.” He attributes the therapeutic value of iodine in tubercu- 
losis to the iodine content of the thyroid gland. Bauer, Turban, 
Muralt, Sergent, Rénon, and others have confirmed these observations. 
In this connection it is important to mention that hypothyroid indi- 
viduals suffer from tuberculosis more often than others, as will be shown 
in another part of this book. 

The etiological relationship between adrenal function and tuber- 
culous disease is even more evident. The low blood-pressure in the 
pretuberculous stage, the myasthenia, weakness, and especially the 
brown pigmentation of the skin, all of which are common symptoms 
of active phthisis, speak for disfunction of the adrenal glands. 
Sajous says that lesions of the adrenal, clinical or experimental, 
increase materially the vulnerability to infection. “In tubercu- 
losis, in fact, adrenal stigmata are very common, 24 per cent accord- 
ing to Lafitte and Moncanny, and 20 per cent according to Laignel- 
Lavastine of cases taken at random having shown more or less bronzing 
—a sign of advanced lesions of the adrenal tissues.’’ Bauer suggests 
that outdoor life, which has been found efficacious in phthisiotherapy, 
usually produces bronzing of the skin, which, according to some 
authors, is an indication of functional activity of the accessory chrom- 
affin tissue, counteracting the tuberculous toxemia. Sergent, Gerald 
Webb, and many others have used adrenal therapy in certain cases 


1 Rev. Méd. de la Suisse Romande, 1895, 15, 241. 
2 New York Med. Jour., 1917, 106, 389. 


PREDISPOSITION OF THE LUNGS 115 


of tuberculosis with good results. Experimentally Gerald Webb! and 
his co-workers have found that tuberculous infection is followed by 
enlargement of the thyroid and adrenals, probably in response to a 
demand for increased function. It must, however, be mentioned in 
this connection that hypofunction of the adrenals, observed in many 
cases of phthisis, is usually due to tuberculous lesions of these glands, 
and may be considered a result of tuberculous disease more than an 
etiological factor. On the other hand, myasthenia, vascular hypo- 
tension, etc., are early symptoms, so early that some writers have been 
tempted to call them “pretuberculous.”’ 

The etiological relationship between gonadal function and tubercu- 
losis deserves careful study. Clinical observations appear to favor 
the view that hypofunction of the sexual glands has a salutary influence 
on existing tuberculous disease. Bauer? speaks of this relationship 
as beyond any doubt. He has never observed a case of tuberculosis 
in a eunuch. Further on we will show that when symptoms of 
eunuchism develop in persons with tuberculosis of the testicles, tuber- 
culosis of the lungs is uncommon. Warnekros has observed this fact 
in castrated women, and Mauthner in castrated guinea-pigs. A very 
large proportion of women who develop pulmonary tuberculosis during 
or soon after the onset of the menopause suffer but little from the 
pulmonary lesion which tends to sclerosis; fibroid phthisis in general 
occurs mainly in persons over forty years of age, when the functions 
of the sexual glands are rather low. On the other hand, during the 
period of puberty, when the sexual glands are at the height of functional 
activity, tuberculosis is apt to run a progressive course. 

We know very little about the etiological relationship of disfunction 
of other endocrines to tuberculosis. 

Predisposition of the Lungs.— More than nine-tenths of all tuber- 
culous disease in humans is found in the lungs; animal experimentation 
also shows that these organs are more likely to suffer as a result of 
tuberculous infection than any other structure. No matter how experi- 
mental infection is accomplished, by subcutaneous or intraperitoneal 
inoculation, by intravenous injection, by inhalation or ingestion of the 
bacilli, there occurs almost invariably a lung lesion sooner or later, 
irrespective of the other organs that may be affected by tubercle. 

Some, notably Bartel,*® believe that this is due to the well-known 
defective development of the pulmonary lymphatic system. The 
lymphatic structures are excellent weapons against all infections, and, 
possessing poorer lymphatics, the lungs are thus more liable to tuber- 
culous changes after the specific virus is brought into them with the 
inhaled air, or the blood stream. ‘Those who favor this viewpoint to 
physiological anthracosis of the bronchopulmonary lymphatics, met 
with in nearly all adult city dwellers, as reducing the functional 


1 Am. Rev. Tuberc., 1921, 5, 266. 
2 Med. Klinik, 1921, 17, 1045. 
3 Pathogenese der Tuberkulose, Berlin, 1918. 


116 PHTHISIOGENESIS 


capacity of these structures. However, clinical experience shows 
clearly that anthracosis does not predispose to tuberculosis in the 
vast majority of cases. In fact, coal miners, whose pulmonary lympha- 
tics are glutted with soot, are less liable to tuberculosis than others 
(see p. 1382). 

The anomalous circulation of blood in the lungs has been considered 
by some as responsible for the frequency of tuberculosis in them. 
It is mentioned in this connection that they are not supplied suff- 
ciently with arterial blood. As will be shown later on, oligemia of 
the lungs, in fact, predisposes to pulmonary tuberculosis, as is the 
case with pulmonary stenosis (see p. 127); on the other hand, in 
pathological conditions involving pulmonary hyperemia, as in mitral 
stenosis, tuberculosis is exceptional. 

Certain investigators have found lung tissue an excellent culture 
medium for the growth of tubercle bacilli. Neumann and Wittegen- 
stein,! A. E. Porter,? and others, have attempted to culture tubercle 
bacilli on various organs and found that while in most tissues the virus 
loses its virulence, in lung tissue it retains it. Porter found that liver, 
thymus, and lymphatic gland were strongly bactericidal, pancreatic 
extract the most powerful, while lung tissue was the least bactericidal. 
It has also been suggested that while in most other organs there is, 
as arule, to be found a lypolytic ferment, the lung lacks it. But Sieber 
and Dzierzgowski’ have shown that this assumption has no foundation 
in fact. In this connection it is interesting that Abderhalden speaks 
of demonstrable ferments in the pulmonary alveoli which, he states, 
have their origin in the leukocytes which migrate into them in large 
numbers to fight invading pathogenic microorganisms. Another sug- 
gestion as to why tubercle bacilli thrive in lung tissue is one pro- 
pounded by M. Weisz! to the effect that it lacks in oxidizing ferments, 
oxydases. The connective tissue in the lungs is known to be deficient 
in nuclei which, in all probabilities, is an adaptation to the oxygen- 
carrying function of the lung. In other words, the predisposition of 
the lung to tubercle is alleged to be the result of the inferior oxidizing 
power of its tissues. Still another suggestion has been made: Tubercle 
bacilli in the lymphatic system enter the veins, and are carried by the 
blood first through the right heart. The lung is the first viscus they 
strike. 

Because of the narrow flat chest seen in many tuberculous patients 
we are apt to think that their lungs are smaller than normal. But 
actual investigations have shown that Rokitansky was right when he 
stated that the lungs in the tuberculous are relativ ely more voluminous 
than in others. It appears that the narrowness and flatness of the 
chest is compensated by its excessive length. In addition there is found 


Beitr. z. Klinik. d. Tuberk., 1909, 12, 145. 
Jour. Hygiene, 1917, 16, 55. 

Ztschr. f. physiol. Chemie, 1909, 52, 254. 
Miinchen. med. Wehnschr., 1912, 53, 697. 


mo tS 


PREDISPOSITION OF THE PULMONARY APICES 117 


a small heart, defective structure of the arterial walls, and a small 
abdominal cavity with correspondingly small abdominal viscera. 
These peculiarities have been observed by many pathologists, and 
Brehmer insisted that the chief characteristic of the phthisical chest 
consists in a disproportion between the voluminous lungs and the small 
heart. The abnormally large lung, with its correspondingly large 
capillary network, is insufficiently nourished by the amount of blood 
which the small heart and hypoplastic bloodvessels can send forth, 
and is thus more exposed to attack by the tubercle bacilli which are 
brought there by the blood or air stream. The comparative immunity 
to tuberculosis of individuals who present stigmata of lymphatism, 
which is discussed elsewhere in this book, is in agreement with the 
hypothesis that an abnormal and defective circulation of the blood in 
the lungs is responsible for its excessive predisposition to tuberculosis. 
The fact that the terminal bronchioles are not supplied with cilia is 
also suggestive. Tubercle bacilli, reaching there with the inhaled air, 
may settle within the air sacks, and are then carried by the lymph 
vessels farther on, until arrested in the lymphatic glands. 

Predisposition of the Pulmonary Apices.—It is, however, important 
to recall that the entire lung is not subject to tuberculous changes, 
excepting in acute miliary tuberculosis and the terminal stages of 
chronic phthisis. The point of election for tuberculous lesions is the 
uppermost part of the lung, the apex, which is in itself an argument 
against the inhalation theory of the disease. A priori we should expect 
that gravity should rather carry tubercle-laden air downward, into the 
lower lobes of the lungs. 

Various hypotheses have been suggested to account for the apical 
localization of phthisis. Some have maintained that it is due to the 
lesser functional activity of the upper part of the chest which expands 
but slightly even in the female, in whom the pectoral region, and not 
the real pulmonary apex, expands during ordinary breathing. 'Tende- 
loo! showed that expansion of the air vesicles differs in the various 
parts of the lungs; it is least in the paravertebral and the uppermost 
parts, and the maximum occurs in the lower and anterior-lateral parts. 
Renewal of air is proportional to the expansion of the air vesicles. 
For this reason, tubercle bacilli brought in with the inspired air, as 
well as with the lymph stream, have more chance of remaining in the 
apices, thus favoring implantation at that point. In the adult the 
uppermost portion of the lung extends for about one to one-and-a-half 
inches above the first rib, and that portion is only covered by soft 
tissues; it is thus deprived of the inspiratory pull of the bony framework 
of the chest, is more exposed to the external atmospheric pressure, and 
therefore any impediment to the exit of the air current, due to any 
cause, also impedes the proper expansion of the apex, and atelectasis 
of this portion of the lung is favored, retaining germ-laden air. While 


1 Studien tiber die Ursachen der Lungenkrankheiten, Wiesbaden, 1902. 


1i8 PHTHISIOGENESIS 


strong respiratory movement of the chest will easily ventilate the lower 
lobes of the lungs, the ventilation of the apices is rather defective for 
the above-mentioned reasons. 

It appears, however, that this mechanical explanation does not 
clear up the problem. We should expect that in pneumokoniosis the 
dust would be retained mainly in the apices, which is not the case. 
In fact, most authorities agree that in pneumokoniosis the upper parts 
of the lungs are comparatively free from deposited dust, while the 
lower and posterior parts may be filled with the aspirated material. 

Other writers attribute the predisposition of the apices to their 
defective circulation. They have not the rich blood supply of the 
lower lobes. In addition, according to Tendeloo, the apices have a 
defective lymph circulation. While all other large bronchi proceed 
from the main bronchi in a straight direction, or at an obtuse angle, 
so that the air can pass straight ahead in either direction during inspira- 
tion and expiration, the apical bronchus forms an almost right angle, 
and the movement of the inspired and expired air is impeded. Diffi- 
culty in the proper ventilation of the apical portions of the lungs is 
thus created. Rindfleisch maintained that the bronchial secretions 
in the apices are thicker and more viscid than in other tubes, because 
of the relative dryness of the apices owing to paucity of the blood, 
the effects of gravity. 

More recently Cobb! suggested, and brought considerable proof in 
substantiation, that the apical localization of phthisis is due to defec- 
tive glandular supply of that part of the lung. Tubercle bacilli, having 
no selective power for any particular portion of lung tissue, will grow 
as rapidly in one portion as in another, once they are arrested and 
gain a foothold. In man, that portion of the parietal pleura lying 
contiguous to the apex of the lung is drained by a vast network of lymph 
vessels that empty into the deep cervical chain. Nowhere else in the 
human thorax is there a decided counter lymph current; and, granting 
that there is this counter current, it could account for an area of lymph 
stasis in the apex of the lung. This is in agreement with the views of 
Tendeloo, and especially Bartel, mentioned above. 

Freund’s Theory of Stenosis of the Upper Thoracic Aperture.— 
About sixty years ago Freund? pointed out that stenosis of the bony 
thorax is very frequently encountered in consumptives, but his obser- 
rations were neglected and soon forgotten, to be taken up again by 
himself, Hart and Harras,? and others. Bacmeister’s‘ experimental 
investigations have finally given great plausibility to Freund’s theory. 

The deformity of the upper thoracic girdle, which may be congenital 
or acquired, consists mainly in an ossification of the first costal cartilage 
and a shortening of the first rib which exerts pressure upon the lung 


1 Jour. Am. Med. Assn., 1918, 70, 1511. 

2 Beitr. z. Histologie d. Rippenknorpel, Breslau, 1858. 

3 Der Thorax phthisicus, Stuttgart, 1908. 

4 Die Entstehung der menschlichen Lungenphthise, Berlin, 1914. 


STENOSIS OF THE UPPER THORACIC APERTURE 119 


apex which it surrounds, thus obstructing the circulation of the blood 
and lymph, preventing the removal of any foreign body—the tubercle 
bacilli—that may be brought there by the blood or the inspired air, 
and favoring its localization at this point. Shortening of the first 
costal cartilage also involves an excessive inclination of the upper 
thoracic aperture toward the spinal column. The sternum lies too 
deeply, the ribs run slantingly downward, the shoulders hang low 
and forward, the scapule protrude like wings, and the result is the 
phthisical chest of the classical authors. 

Freund, Hart, and Harras have studied the tuberculous thorax 
on the autopsy table and in the living with the aid of roentgenography, 
and have found that stenosis of the upper aperture is very frequent. 
The abnormal shortening of the first rib makes the transverse diameter 
short, converting the human thorax into one like that of the lower 
animals, and to a certain extent infantile, as is shown in Fig. 15. The 
narrowing usually occurs at the latero-posterior bulging, exactly where 


a 
> 
.y 
TA See 
Fie. 15.—Diagrammatic representation of the upper aperture of the thorax: a, the 
primary form (animals, primitive human form); b, secondary form (adult man). (After 


Wiedersheim.) 


the apices of the lung are surrounded by the first rib, which under 
these conditions compresses the pulmonary tissues beneath. This 
deformity may occur unilaterally or bilaterally, but the end-result 
is always the same—narrowing and rigidity of the upper thoracic 
girdle with resulting compression of the lung. 

Independent of Freund, Schmor!! found a groove about 2 cm. below 
the highest point of the apex of the lung. This groove is very frequently 
encountered in newborn infants, but in them it can be obliterated when 
the lung is inflated. During adolescence it disappears in persons with 
normal chest walls. In most persons in whom it persisted Schmorl 
found tuberculous lesions beneath the point which was pressed upon 
by the shortened rib (Figs. 17 and 18). 

These observations have been confirmed by Birch-Hirschfeld? from 
another point of view. While searching for the initial lesion of tuber- 
culosis in cadavers dead from other diseases, he found that phthisis 


1 Miinchen. med. Wehnschr., 1902, 48, 1995. 
2 Deutsch. Arch. f. klin. Med., 1899, 64, 58. 


120 PHTHISIOGENESIS 


begins in the walls of a bronchus of the third to the fifth order, and 
ascribed it to certain pressure exerted on these tubes, preventing the 
exit of air and secretions. This bronchiole, which Clifford Allbutt 














Fic. 16.—Upper aperture of the thorax: A, normal on left side; B, narrowed at the 
right. (Freund.) 





Fig. 17.—Right lung. (His’s model.) The Fig. 18.—Left lung. The groove of the first 
indentations made by the ribs are shown. The rib is shallower than in the right lung. 
first groove is the indentation made by the first 
rib and is known as Schmorl’s groove. 


STENOSIS OF THE UPPER THORACIC APICES 121 


ealls “Hirschfeld’s bronchiole,” from its position and nature favors 
that secretions, instead of clearing themselves automatically, will 
stagnate more or less if pressed upon to a greater or lesser degree by 
the first rib, located as it is on the apex, leading spirally against the 
action of gravitation upward, outward, and backward. 

Finally, Bacmeister’s! investigations have apparently confirmed 
these anatomical, pathological, and clinical findings. He surrounded 
young and growing rabbits with a wire loop at the first costal ring. 
thus causing stenosis of the upper aperture of the bony thorax. The 
pulmonary apex was thus compressed, and a groove was indented in 
the lung beneath the wire loop corresponding to the one observed by 
Schmorl in human consumptives. Infecting these animals, he pro- 
duced isolated and localized pulmonary tuberculosis, while in normal 
animals, used as controls, infection produced miliary tuberculosis, 
but never localized tuberculosis of an apex. In this manner he could 
produce local tuberculous lesions on either side of the chest, or 
bilaterally. 

Considerable clinical evidence has been brought in support of this 
theory. In children the upper aperture of the thorax is very elastic, 
and therefore apical phthisis is exceedingly rare; when infected, the 
tracheobronchial glands are affected, or general miliary tuberculosis 
is the result. During the period of puberty, when the spinal column 
grows and raises the upper thoracic girdle, permitting the first rib 
to exert pressure on the pulmonary apex, typical phthisis may occur. 
The largest number of cases of active tuberculosis of the lung, though 
not the largest number of deaths due to this cause, occur between 
fifteen and thirty years; between thirty and forty the proportion 
diminishes, and between forty and sixty there again occur a large 
number of cases. Hart explains these phenomena in this manner: 
During puberty and soon thereafter any congenital or acquired shorten- 
ing of the first rib becomes dangerous to the individual because the 
growing apex of the lung finds itself enclosed in the small and rigid 
thoracic cavity, which does not grow in the same proportion as the 
lung, and the shortened first rib compresses it, thus favoring tubercu- 
lous degeneration. After forty, when ossification of the costal cartilage 
is, to a certain extent, normal, conditions are again favorable for the 
development of phthisis. 

While several authors have confirmed these findings by Freund and 
Hart, it appears that careful observers have looked for stenosis in the 
upper thoracic aperture while making autopsies, or roentgenographing 
tuberculous subjects, and could not find it in an unusually large pro- 
portion. Schulze, Smith, Neumann,” and finally Wenckenbach, have 
all obtained negative results. Roentgenography of 273 tuberculous 
individuals by Neumann has not shown abnormal shortness, or 
excessive ossification of the first rib and cartilage. Among 238 cases 


1 Mitt. a. d. Grenzgeb. d. Med. u. Chir., 1913, 26, 630. 
2 Beitr. z. Klinik. d. Tuberkulose, 1919, 40, 1. 


122 PHTHISIOGENESIS 


of tuberculosis, Wenckenbach! found that 35.7 per cent showed no 
trace of ossification of the first cartilage, 25.5 per cent a slight ossifica- 
tion which is normal in healthy individuals over thirty years of age. 
It is thus seen that in 61.75 per cent of tuberculous subjects this ossi- 
fication cannot be credited with etiological relationship to the tuber- 
culous process in the lungs, and that only in 17.2 per cent has this 
anomaly been found to exist. In younger individuals it is even less 
frequently found. Thus, among 172 cases of tuberculosis in persons 
between fifteen and thirty years of age, it was found only in 1.5 per 
cent, while in 86.8 per cent no trace of the mentioned anomaly could be 
discovered. 

Arthur Keith,? Stiller,? and other authors are inclined to look upon 
this deformity of the thoracic girdle rather as a result of tuberculosis 
than a cause of it. Pottenger* points out that the muscle change 
described by Freund as hypertrophic and due to overwork, caused by 
the muscle pulling against an ankylosed rib, is more likely a contrac- 
tion of the muscle caused by the inflammation within the lung reflexly 
through the spinal cord. 

Constitutional Inferiority.— Many writers have maintained that pre- 
disposition to tuberculosis is not specific, due to anomalous structure 
or function of a given organ, but that it is general. They claim that 
the majority of tuberculous patients present signs of constitutional 
inferiority; others allege that “stigmata of degeneration,” in the sense 
given this expression by Lombroso, are preponderating. 

The application of the term dégenéré to tuberculous individuals was 
first made by the noted French clinician Andral, and Féré stated that 
the phthisical present very frequently stigmata of degeneration. Then 
a Polish writer, Polansky,’ made some extensive, though not very 
astute, observations along these lines, while making autopsies on 854 
tuberculous subjects. Among the numerous anomalies and stigmata 
which he said were common among these subjects are concavity of 
the region of the small fontanelle, persistence of the interfrontal suture 
to an advanced age, frequent occurrence of Wormian bones, abnormal 
length of the transverse processes of the lower cervical vertebree, bifid 
spinous processes in the lower dorsal and upper lumbar vertebre, etc. ; 
also bifurcation of the xiphoid cartilage, or its perforation. He also 
claims that certain anomalies in the viscera are excessively found, such 
as hypoplasia of the cardiac muscle, lack of the middle lobe of the right 
lung, thinness and narrowness of the wall of the aorta, bifurcation of 
the aorta as high as the second or third lumbar vertebra, lobulation 
of the kidneys and liver, abnormal length of the right lobe of the liver, 
double ureters, accessory spleens, fetal length of the stomach, abnor- 


1 Wien. klin. Wehnschr., 1918, 31, 379. 

2 Further Advances in Physiology, 1909. 

3 Berl. klin. Wchnschr., 1912, 49, 97. 

4 Muscle Spasm and Degeneration, St. Louis, 1911. 
5 Ztschr. f. Tuberk., 1904, 6, 140. 


CONSTITUTIONAL INFERIORITY 123 


mally long colon, mesocolon and appendix, Meckel’s diverticulum, 
patency of the hernial canals, etc. Excessively long extremities, and 
heterosexual distribution of the hair on the body are other anomalies 
mentioned by this writer. 

Many other authors have found signs of constitutional inferiority 
among the tuberculous. A Japanese writer, Iwai! found polymastia 
and supernumerary nipples; Rosolimo? absence of the lobule, the so- 
called “jug-handle” ear; and Holeman? says that he observed stigmata 
of degeneration; “the most common, as well as the most striking and 
easily observed, are various malformations of the pinna; next to these, 
ill-formed palates and gross facial asymmetries abound.” W. C. 
Rivers‘ published a book showing that certain atavistic tendencies are 
found in a large proportion of consumptives, notably icthyosis, man- 
cinism, squint, ete. 

The asthenic constitution, which has been described in detail by Stiller, 
is said by some authors to be predisposing to tuberculous disease. 
People of this type have long chests and necks, winged scapule, pro- 
truding clavicles and second rib, and very defective and hypotonic 
musculature, involving ptosis of the abdominal viscera, etc. In this 
country, Joel E. Goldtwait® has arrived at the conclusion that “the 
congenital viscero-ptotic, the carnivorous, the hyper-onto-morph”’ is 
very much subject to tuberculosis. 

The complexion of the individual also has been considered in this 
regard. Some 2000 years ago Hippocrates said that blondes are more 
likely to develop consumption than brunettes. Recently others have 
maintained the same. Red hair is especially said to be predisposing 
by Rivers,® Bauer,?7 and many others. Schmidt states that “hair 
disharmony,’—bright red mustache, with dark drown hair on the 
head—is found in excessive proportion in patients with tuberculous 
peritonitis. 

These anomalies of pigmentation are due to ethnic inter-mixtures. 
We have seen that racial peculiarities have very little to do with 
tuberculous infection, excepting in so far as to the length of time a 
given ethnic unit has been exposed to tubercle bacilli (see p. 73). 
But many writers have maintained that consanguineous marriages are 
predisposing to tuberculosis in the offspring. However, a more recent 
author, Herman Lundborg,’ found that races that avoid intermixture 
are more or less immune; and wherever racial miscagenation is intense 
the tuberculosis morbidity and mortality are high. This does not hold 


1 Lancet, 1907, 2, 958. 

2 Wien. klin. Wchnschr., 1908, 31, 790. 

3 Med. Record, 1915, 88, 1037. 

4 Three Clinical Studies in Tuberculous Predisposition, London, 1917; Lancet, 1921, 
p. 319. 

5 Boston Med. and Surg. Jour., 1916, 175, 88. 

6 British Jour. Children’s Dis., 1920, 17, 59. 

7 Konstitutionelle Disposition zu inneren Krankheiten, Berlin, 1917, p. 54. 

8 Swenska Likarsillskapets Handlingar, 1920, 46, 73; abstr. in Zentralbl. f. Tuber- 
kuloseforschung, 1921, 15, 338. 


124 PHTHISIOGENESIS 


good for the white population of the United States nor will those who 
correlate anthropological with demographic data anywhere in the 
world agree with this view. 

Other anatomical anomalies are those pertaining to the structure of 
the lymphatic system. Virchow, and later, Cornet, stated that certain 
individual variations in the lymphatic system render infection and the 
subsequent evolution of tuberculous disease easier. Geddes! also main- 
tains that the venous and the lymphatic systems are of defective 
development in the tuberculous. 

Clinicians, who care for and observe thousands of cases of tubercu- 
losis have not noted that “stigmata of degeneration” are more common 
among them than among others. Considering that tuberculosis is 
extremely widespread, affecting nearly one-tenth of humanity, It is 
clear that among tuberculous patients there are many who present 
stigmata of constitutional inferiority. But it cannot be truthfully said 
that they preponderate. Indeed, it appears that when perfect speci- 
mens of physical development are affected, the disease, as a rule, 
pursues a very malignant course. 


PREEXISTING DISEASES. 


Disease of the Respiratory Tract.—Of the diseases which, at one 
time or another, have been considered predisposing to the develop- 
ment of pulmonary tuberculosis, those affecting the upper respiratory 
tract are nearly always mentioned as preparing a favorable soil for 
the implantation of tubercle bacilli. Thus, we occasionally meet with 
instances of bronchiectasis, syphilis, actinomycosis, and cancer of the 
lungs, and chronic pneumonia, in which tuberculosis is implanted at 
the site of the primary disease. There are two plausible explanations 
for these phenomena: In most cases it is, in all probability, an old, 
dormant tuberculous lesion, dating back to childhood, that is reawak- 
ened into activity by the intercurrent disease, assisted perhaps by the 
reduction in the vitality and resisting powers of the patient. In pneu- 
mokoniosis the foreign particles in the lung tissue are said to produce 
local ischemia, obstruct the lymph channels, and thus prevent ab- 
sorption, or destruction, of any tubercle bacilli that may be brought 
in by the air stream. But, as will be shown later on (see p. 132), there 
are good reasons for speaking of a comparative immunity against 
tuberculosis by persons affected with the just-mentioned diseases. 
Real lobar pneumonia is hardly ever followed by pulmonary tubercu- 
losis, and in most cases in which it has been observed, the probabilities 
are in favor of the primary disease being acute pneumonic phthisis 
which had subsided, then pursuing the course of chronic tuberculosis. 
“specially is this true of “apical pneumonias” and “basal tubercu- 


1 Dublin Jour. Med. Sci., 1909, 128, 337. 


PREEXISTING DISEASES 125 
losis,’ and many of the so-called unresolved pneumonias, when not 
empyemata, have been tuberculous from the start. 

Pleurisy.—Of greater importance is the etiological relation of 
pleurisy to phthisis. Of course, the secondary pleurisies, those occur- 
ring in cases of intrathoracic neoplasms, cardiac and renal diseases, 
have no significance in this regard. But the forms of acute and chronic 
pleurisy which had formerly been considered “idiopathic,”’ appear to 
be, in the vast majority of cases, of a tuberculous nature, though many 
are undoubtedly rheumatic. 

Strictly speaking, pleurisy cannot be considered predisposing to 
pulmonary tuberculosis, because it is in itself a manifestation of 
tuberculous disease. As will be shown later on (see Chapter X XVI), it 
is due to tubercle bacilli, and indicates that the acute or annoying 
manifestations of the pathological process begin in the pleura. 

Diseases of the Upper Respiratory Tract.— Because acid-fast bacilli 
are at times found in the tonsils, many writers have argued that this 
gland is one of the main channels of entry of the virus of tuberculosis, 
and that diseases of the rhinopharynx are predisposing to tuberculous 
disease of the lungs. 

Clinical experience is, however, not in agreement with this view. 
The fact that virulent tubercle bacilli are at times found in the tonsils 
does not prove that they can pass further on into the deeper respira- 
tory passages and cause local lesions in the lungs, as was already 
shown. Moreover, it is exceedingly rare that pulmonary tuberculosis 
should begin with an acute inflammatory process in the nose and 
throat. This point is discussed in greater detail in Chapter XXX. 
On the whole, it may be stated that no etiological relationship between 
acute and subacute inflammatory processes of the nose and throat 
and pulmonary tuberculosis has been found to exist. 

‘‘Colds.’’— Clinical observation shows clearly that exposure to cold, 
or chilling the body, very often precedes the onset of active symptoms 
of pulmonary tuberculosis. Of course, it is self-evident that chilling 
cannot produce tuberculous disease. But when we bear in mind that 
practically everybody has tubercle bacilli in some part of the respira- 
tory tract, we can readily understand that the changes induced by 
exposure to cold may be instrumental in preparing a favorable soil for 
the reactivation of dormant tubercle bacilli. A large proportion of 
the patients in whom the onset of tuberculosis was marked by symp- 
toms of pleurisy state distinctly that they had felt well until exposure 
while sea-bathing, or emerging from an overheated room into a cold 
or windy atmosphere, or being chilled by wet and cold clothing. In 
active cases of tuberculosis, complicating pleurisy is very frequently 
observed after exposure to the vicissitudes of the weather. To be sure, 
we are in the dark as to the exact pathological or biochemical mechan- 
ism of “catching cold.”’ It isimmaterial for our purposes whether the 
primary changes in the affected tissues are those of active or passive 
hyperemia, as has been supposed for a long time, or a reflex vaso- 


126 PHTHISIOGENESIS 


constriction and ischemia, as has been found experimentally by Mudd 
and Grant,' or the more recent theory of Schade,? that functional 
disturbances in the cells of the tissues of a colloidal character, are 
responsible. No observant clinician has failed to be impressed with 
the fact that a large proportion of known tuberculous patients are 
distinctly harmed by exposure to cold, or chilling of the body, and 
many who did not consider themselves sick at all, began to show 
symptoms of tuberculosis soon after exposure and chilling. It is clear 
that in the latter class of cases, of which we meet many, tubercle 
bacilli were present in the thoracic organs, especially the lungs, glands, 
and pleura. But the chilling is here the exciting cause, reactivating 
dormant lesions which had given no trouble before. On this point 
many recent writers, notably Sticker,’ Mohr,‘ Aufrecht,® Keysser,® 
Ransome,’ and many others agree. It is unfortunate that, absorbed 
in bacteriology, we are apt to underestimate the predisposing, and often 
the exciting element of exposure to the vicissitudes of the weather in 
the etiology of tuberculous disease of the lungs. 

There is one point to be remembered by physicians in this connec- 
tion. When reactivating dormant tuberculosis of the lungs, exposure 
does not produce symptoms of the “common cold” such as those of 
coryza, rhinopharyngitis, tonsillitis, ete. The symptoms following 
exposure in these cases are those of incipient tuberculosis, such as 
cough, fever, etc., and when the pleura is involved, which is very 
frequently the case, symptoms of pleurisy are at once manifest. 

Chronic Bronchial and Pulmonary Diseases.— Clinical experience 
has shown conclusively that chronic diseases of the bronchi and lungs 
are not predisposing to tuberculosis. The notion of some patients, and, 
at times, of physicians, that a “neglected” bronchial catarrh, asthma, 
pulmonary emphysema, etc., is at any time liable “to turn into con- 
sumption” seems to be unfounded. ‘To be sure, there are many patients 
who have coughed for months or years before they have been pronounced 
tuberculous, but the cough, expectoration, dyspnea, etc., were, in these 
cases, due to quiescent, or even active, but unrecognized, tuberculosis. 
What is called chronic bronchitis, is in most cases secondary to cardiac 
or renal disease. As will be shown later on (see Chapter XXX), there 
is ample evidence to the effect that pulmonary emphysema and asthma 
are only rarely followed by tuberculosis. Exceptions that may be 
mentioned are the emphysematous forms of fibroid phthisis, which are 
due to the inhalation of certain kinds of dust, especially in miners of 
silica and certain metals, notably copper and tin, also in garment 
workers, furriers, rag-pickers, ete. 

1 Jour. Med. Research, 1919, 40, 55. 

2 Miinchen. med. Wehnschr., 1919, 66, 1021; 1920, 67, 449. 

3 Erkaeltungskrankheiten und Kaelteschaden, Berlin, 1916, pp. 141, 197. 

4 In Mohr und Staehelin’s Handbuch d. inn. Medizin, 1912, 4, 759. 
Ztschr. f. Aerztl. Fortbild., 1917, 14, 574. 


5 
6 Ztschr. f. Baneologie, 1913, 6, 421, 455, 
7 Lancet, 1888, 1, 762. 


PREEXISTING DISEASES 127 


Diseases of the Heart and Bloodvessels.— ‘The small heart seen in 
a large proportion of tuberculous patients has suggested that there 
may be an etiological relationship between tuberculosis and the size, 
capacity and thickness of the walls of this organ. Many authors con- 
sider a congenital hypoplasia of the cardiac muscle a prerequisite, or 
at least a predisposing factor, in tuberculosis. Moreover, with an 
hypertrophied heart, active tuberculosis of the lungs is exceedingly 
rare. The reason for this phenomenon is given as follows: Conditions 
of the heart which produce oligemia of the lung seem to favor the devel- 
opment of tuberculosis, and this is perhaps best illustrated by the 
fact that nearly all who have congenital heart disease, pulmonary 
stenosis, suffer from and succumb to tuberculosis. On the other hand, 
diseases of the heart which produce congestion and plethora of the 
pulmonary bloodvessels, as is the case in mitral stenosis, are antagonis- 
tic to tuberculosis. The fact that tuberculosis is very rare in patients 
with mitral stenosis favors this view. The clinical aspects of this 
problem are discussed in Chapter XXX. 

Acute Infectious Diseases.—It has repeatedly been observed that 
the endemic contagious diseases, like measles, scarlet fever, whooping- 
cough, diphtheria, etc., are often followed by phthisis, and in infants 
and children tuberculous bronchopneumonia is frequently a sequel of 
measles and whooping-cough. This heightened predisposition may 
be explained as depending on the general disturbance in health caused 
by the fever, catarrh of the respiratory passages, etc., which reduce 
the resisting power and produce a soil favorable for the activation of 
dormant foci of tubercle bacilli, or favor new infections. These diseases 
are accompanied to a great extent by irritation of the mucous mem- 
branes and defects in the epithelium which facilitate the entrance of 
the bacilli, so that infection of the respiratory passages is particularly 
favored. The influence of measles and whooping-cough may be purely 
mechanical; fits of violent cough are liable to rupture tuberculous 
glands in the chest. 

In children tuberculous bronchopneumonia is very frequently ob- 
served to follow an attack of measles. In adults our experience had 
been limited till the epidemic which broke out in various camps in 
which United States soldiers were stationed during 1917-18. Among 
5945 cases of measles in soldiers it was found that 173, or 2.91 per cent., 
had developed active tuberculosis. George E. Bushnell is inclined to 
the opinion that the measles reactivated latent tuberculous foci, though 
he believes that it is probable that the number of really tuberculous 
cases was less than the above figures would indicate. Some of these 
cases Classed as tuberculous were rather cases of unresolved pneumonia. 
But, on the other hand, he has no doubt that all cases of tuberculosis 
reactivated by measles had been detected at the first examination of 
these soldiers. This may be considered an experiment on a large scale 


1 Jour. Am. Med. Assn., 1918, 70, 1823. 


128 PHTHISIOGENESIS 


which tends to show the influence of measles on the incidence of 
tuberculosis. 

That these diseases may be strong predisposing factors to tubercu- 
lous infection and the extension of existing tuberculous disease, was 
shown from another viewpoint. “ Allergy,’! or the altered reactivity 
of the organism to tuberculin, is apparently dependent upon the fact 
that the body has produced antibodies which counteract the effects of 
tuberculous toxemia, and is diminished in intensity, or disappears 
altogether, during an attack of measles. We then have “anergy,” 
which indicates that resistance to infection has diminished, just as in 
far-advanced phthisis for a short period before the fatal termination, in 
miliary tuberculosis, ete., when all defensive powers have failed. Von 
Pirquet has named this state “anergic,”’ 7. e., non-reacting. He assumes 
that the measles process occupies the antibodies which are needed for 
the repulsion of the tubercle bacilli present in the body. During this 
unprotected period the tubercle bacilli can grow and pass through the 
necrotic walls of a caseous gland, or secondary diseases can also occur, 
because now the circulating tubercle bacilli can find favorable condi- 
tions where at other times they would have been destroyed. He draws 
an analogy between this condition and the condition favoring the prog- 
ress of tuberculosis in the adult—general debility due to malnutrition, 
overwork, or any other condition robbing the body of its natural 
defences. 

Influenza.— The connection between influenza and phthisis is even 
less clear. During the great pandemic of influenza in 1891 it was 
observed that the mortality was increased, and similar. observations 
had been made before. Arthur Ransome? called attention to the 
periodic waves in the death-rate from phthisis in England and Wales, 
and noted faint indications of a rise in 1853, 1866, 1878 and 1890. 
Bulstrode, in referring to these rises in the mortality, pointed out that 
there was an outbreak of influenza in 1855 which might possibly account 
for the increase in tuberculosis at that time. But in 1866 the cotton 
famine accounts for it much better. During 1890-91-92, and again 
in 1899-1900, the mortality from phthisis increased as a concomitant 
to epidemics of influenza. As Newsholme’ points out, the experience 
of 1917-18 was the third occurrence in recent years of this coincidence, 
and there can be no doubt that influenza is a most dangerous complica- 
tion of pulmonary tuberculosis. But during the two years following 
the epidemic the tuberculosis mortality declined in England. During 
the epidemics of influenza in the United States in 1918-1919, I observed 
that those who recovered showed no tendency to develop phthisis, 
unless they had tuberculous lesions before the attack of influenza. As 
will be shown elsewhere (see Chapter XXX), when a tuberculous 
person is stricken with influenza, the outlook is not invariably bad. 


1 See von Pirquet, Allergie, Ergebnisse d. inn. Med. u. Kinderheilk., 1910, 5, 459. 
2 Tr. Epidemiol. Soc., London, 24, p. 252. 
3 Lancet, 1917, 2, 591. 


OCCUPATION 129 


Typhoid Fever.— Typhoid fever also has been considered as predis- 
posing to phthisis because of the rather high proportion of consumptives 
who give a history of having passed through an attack of it. Recently, 
Charles E. Woodruff! has discussed the subject in great detail and 
arrived at the conclusion that typhoid fever heads the list of predis- 
posing causes of tuberculosis. The fact that during recent years the 
mortality from tuberculosis and from typhoid has been declining at 
almost the same rate is considered a strong argument. “The three 
diseases ee seem be most frequently followed by tuberculosis 
hooping-cough, and typhoid—are all compli- 





cated with bronchitis,” 

There appears to be a lack of evidence in support of these conten- 
tions. The fact that the mortality-rates from typhoid and phthisis 
run parallel does not prove that the same cause is operative in both 
cases. The somewhat excessive number of consumptives who have 
a history of typhoid does not convince in this direction. It is well 
known to clinicians that acute tuberculosis very often simulates 
typhoid in a striking manner, and with all our diagnostic methods it is 
often very difficult to differentiate the two diseases. In many cases of 
alleged typhoid preceding phthisis I have been convinced that it was 
an acute exacerbation of latent tuberculosis which was mistaken for 
typhoid, just as many attacks of “ grippe’”’ are in reality acute exacerba- 
tions of chronic or mild forms of phthisis. Typhoid fever, like most 
other febrile diseases, may, however, activate latent phthisis, which 
might not have taken an acute or subacute course otherwise. But 
under the circumstances we cannot consider typhoid per se as predis- 
posing to tuberculosis. 


OCCUPATION. 


Of the factors which have been mentioned as predisposing to, or 
at times activating, dormant tuberculosis, the character of the occu- 
pation of the patients has been given considerable attention by many 
writers. Considering the important industrial, sociological, and eco- 
nomic bearings of this problem, it is clear that there have been quite 
some differences of opinion as to the dangers of certain occupations 
in this regard. John Brownlee, a rational statistician and demographer, 
says: “With regard to the influence of occupation, a note of warning 
may perhaps be sounded. The whole field is a very difficult one, and 
the interpretation of the figures, unless the greatest care is exercised 
in drawing deductions, not less dangerous than the interpretation of 
the Holy Scriptures.” 

The main difficulty is that statisticians commonly take the rough 
figures from the death reports and calculate the coefficient of mortality 
according to the occupations of the deceased, without inquiring how 
long the deceased had been working at the given occupations. Many 


1 Am, Med., N.S., 1914, 11, 17. 


150 PHTHISIOGENESIS 


people suffering from chronic phthisis change their occupations, and 
after death the last occupation is registered, while the one that may 
really be responsible for the reactivation of the disease is not mentioned. 

The process of social selection, which is very pronounced in this 
respect, is usually not considered. Thus, as has been pointed out by 
Cobbett, hotel servants in England show a very high tuberculosis 
mortality. Some would be inclined to attribute it to their indoor life, 
as well as to their proclivity to drink alcoholic beverages excessively. 
But others working indoors, in the garment industries, for instance, 
have not an excessive tuberculosis mortality. No doubt there is a 


1 Rates 
Million 


File Cutters, 
‘Tool nitacée es turer y 


Stone & Slate 
Quarr Yniede 


Fostone 
wasone 





; els ‘iod 
er15 20 





Fic. 19.—Mortality from pulmonary tuberculosis, 1900-1902 in certain occupations in, 
England and Wales. (Brownlee.) 


process of social selection going on. Occupations which do not require 
excessive muscular exertion are likely to attract the weakly and the 
sick—among them many with latent or quiescent tuberculosis. For 
this very reason policemen are less liable to develop tuberculosis—only 
strong men are taken into the service. 

Another illustration is brought by Brownlee.t After the age of 
thirty-five, the mortality from phthisis among persons included in the 
class of commercial clerks, and in the class of carmen, carriers, etc., 





1 An Investigation into the Epidemiology of Phthisis in Great Britain and Ireland, 
London, 1918, p. 15. 


OCCUPATION 151 


are practically identical with the mortality of males in general. Before 
this age there is considerable excess of phthisis among carmen, etc. 
It is hardly likely that these variations are to any extent occupational. 
It is much more probable that the occupations have been originally 
selected for reasons of physical fitness, or the reverse. This is con- 
firmed when phthisis mortalities among commercial travelers are con- 
sidered. In this case the mortalities from phthisis are practically 
identical throughout the general population, though on a slightly lower 
level. As commercial travelers are largely chosen from the clerk class, 


Death Rates 
per Million 


16,000 


15,000 
14,000 - 
13,000 |- Tin Miners 
12,000 |- 
11,000 


10,000 


Stone & Slate 
Quarrymen 
Ry 





\ | 
50 55 660 





Fig. 20.—Mortality from pulmonary tuberculosis 1900-1902 among miners in England 
and Wales. (Brownlee.) 


it would seem to be indicated that the fit are put upon the road and 
the unfit kept upon the stool. 

Occupations may predispose to tuberculosis by the dust created, 
and which the workers are compelled to inhale, while working at the 
industry; by dangerous fumes or odors emanated from the material 
used; and also, as we shall see later on, by keeping the workers in 
unclean factories and mills, paying them low wages, etc., all of which 
reduces their vitality and resisting powers. 

Dust as an Etiological Factor in the Evolution of Phthisis.— Because 
pulmonary tuberculosis has been considered a disease caused mainly 


132 PHTHISIOGENESIS 


by inhalation of the virus, dust has been mentioned as an etiological 
factor by writers on the subject for centuries. In nearly all treatises 
on tuberculosis, or on occupational diseases, it is never omitted to 
state emphatically that persons pursuing occupations at which they 
are exposed to the inhalation of mineral, metallic, vegetable, or animal 
dust are more likely to contract tuberculosis, and die from it, than 
others. A few figures, culled from Frederick L. Hoffman’s recent 
monograph,! will supply drastic illustrations of the great dangers of 
contracting tuberculosis of those exposed to the inhalation of certain 
kinds of industrial dust. During 1908 and 1909 the proportionate 
mortality from pulmonary tuberculosis in the United States Registra- 
tion Area was 14.9 per cent of all deaths among all occupied males, 
and only 8.7 per cent among farmers, planters, and farm laborers. 
Among workers exposed to metallic dust, it was 21 per cent; among 
engravers, 31.1 per cent; among printers, lithographers, and pressmen, 
29.5 per cent; among tool and cutlery makers, 24.1 per cent; among 
jewelers, 17.8 per cent; among iron and steel workers, 14.9 per cent. 
Those working in industries exposing them to the inhalation of certain 
kinds of mineral dust are even more menaced by tuberculosis: 21.3 
per cent of the workers at these industries succumbed to this disease; 
potters, 34.6 per cent; glass-blowers, 32.1 per cent; marble and stone 
cutters, 30.7 per cent; plasterers, 16.7 per cent; brick and tile makers, 
12 per cent; coal miners, 9 per cent. Similar statistical evidence is 
available for other countries, notably England and Wales, Australia, 
Germany, France, ete. 

Menacing Kinds of Dust.—From the few figures just brought 
together it is evident that not all kinds of dust are etiologically related 
to pulmonary tuberculosis. Among coal miners tuberculous phthisis 
is relatively uncommon, though they undoubtedly inhale large quan- 
tities of mineral dust, which almost invariably reaches the deeper 
respiratory passages, and remains there, as is evident from the fre- 
quency of pneumokoniosis among them. [uban, as far back as 1863, 
drew attention to this fact and said that in France “coal dust is unable 
to cause pulmonary tuberculosis, or even to favor the evolution of this 
disease.”’ In England, Oliver shows that the same condition prevails, 
and Brownlee says that “ phthisis is a comparatively uncommon disease 
among coal miners.’’ Newsholme brings evidence to the effect that 
coal miners in Derby and Nottinghamshire stand high on the list as 
to expectation of life, being only surpassed by farmers, agricultural 
laborers, teachers, etc. In the United States available evidence is to 
the same effect. Carr, whose experience among miners in the largest 
coal mining towns in Southern I[]linois extended over twenty-five years 
said that ‘bituminous coal miners, while actively engaged in their 
occupation, are practically immune from tuberculous disease.’’ He 
inquired among 600 practising physicians in the coal mining towns of 


! Mortality from Respiratory Diseases in Dusty Trades, Washington, 1918. 


OCCUPATION 133 


this country and, out of some 200 replies received, about 75 per cent 
sustained the point of view that “during active service in his occupation 
the bituminous coal miner is immune to tuberculosis, wholly, or in 
part.” The reservation “during active service,’ of course, indicates 
that the immunity is limited, because tuberculous persons leave the 
mines. But available evidence seems to show that tuberculosis is not 
excessively common among coal miners, despite the fact that coal dust 
penetrates the deep respiratory passages. 

More noteworthy is it that street-sweepers and coachmen, in spite 
of exposure to excessive inhalation of dust, are not excessively liable to 
phthisis. Cornet concluded from this fact that the dangers of tuber- 
culous infection in the street are nil. Sommerfeld has shown that in 
Berlin the street-sweepers have only half the rate of mortality from 
phthisis when compared with the mortality of the working classes in 
that city. In New York City, where several years ago considerable 
agitation was made in favor of protecting the street-sweepers against 
an excessive morbidity and mortality from tuberculosis, statistics have 
not borne out these contentions. Hoffman’s statistics, gathered for 
a monograph on the excessive mortality from consumption in occupa- 
tions exposed to municipal and general dust, show clearly that “the 
recorded mortality from consumption among men in this employment 
is not decidedly excessive.” 

Another kind of dust which is apparently harmless in regard to 
phthisiogenesis is limestone, and also plaster of Paris. In England 
it has been found, according to Collis,! that masons in districts where 
limestone is worked do not suffer from phthisis in excess, while masons 
in districts where sandstone is worked are peculiarly liable to suecumb 
to this disease, and have a shorter prospect of life. Halter and Garb 
have recorded the same to be a fact in Germany, and Fisac? reports 
that in Spain the workers in quicklime and plaster of Paris are immune 
to tuberculosis despite the fact that they live in squalid dwellings, and 
are underfed. He believes that their immunity is due to the inhalation 
of dust containing lime. Hoffman’ brings considerable evidence to 
this effect from among the workers in lime in the United States. 
Several writers have suggested the utilization of lime in the therapeutics 
of tuberculosis. 

Effects of Inhaled Dust on the Pulmonary Tissue.— Barring the few 
kinds of dust just mentioned, it appears that the inhalation of dust 
is a strong predisposing factor in the evolution of tuberculous lung 
disease. In considering the menace of dust it must first be taken into 
consideration that nature has placed many barriers in the way of even 
fine dust entering the deep respiratory passage with the inspired air 
(see p. 50); even when reaching the mucous membranes of the bronchi 
and lungs the latter are not very tolerant of foreign bodies, and most 


1 Public Health, 1915, 28, 252, 292. 
2 Rev. de hyg. de tuberc., 1909, 5, No. 54. 
3 Loe. cit., -p. 217. 


134 PHTHISIOGENESIS 


of it is soon expelled with the cough and expectoration which it pro- 
vokes. However, Moritz found that the sensibility of the mucous 
membrane of the respiratory tract, from the nose to the trachea, is 
reduced in persons working as grinders in a steel factory in Germany. 
Large masses of metallic dust could be seen lying on the vocal cords 
and the mucous membrane of the trachea without provoking cough 
to expel it. For this reason some dust remains, and it is taken by the 
lymph channels and carried farther on. But after persistent deposits 
of dust in the alveoli, the irritation it produces excites a reactive 
inflammation, clogs the lymph channels, and lowers the resisting 
powers of the inv eo lung, preparing the soil for the deposit of tubercle 
bacilli which may thrive in defective tissues. The glands of the lungs 
normally act as filters which retain the dust brought in by inhalation, 
but if new deposits are repeatedly brought into these glands, they are 
ultimately damaging to the structure and function of the lung, impair- 
ing the glands as filters. 

On the other hand, Lubarsch! is of the opinion that clogging of the 
pulmonary lymphatics by coal dust is preventive of tuberculosis for 
another reason. The devitalized tissue is a poor soil for the growth 
of the microorganisms. Then, bearing in mind that extension of tuber- 
culous lesions in the lungs commonly takes place along the lymph 
channels, it is clear that when these are damaged and clogged, they 
prevent the extension of the pathological process. He points out that 
the process is thus purely mechanical, and not biochemical. In a cer- 
tain coal region where he found that the miners show only one-half 
the tuberculosis mortality-rate when compared with the general popu- 
lation, this is only true of pulmonary tuberculosis. Tuberculosis of 
the bones and joints is just as frequent among them as among others. 

This may be true of pneumokoniosis produced by coal dust. But 
in the case of other forms of dust, other factors are at work. In some 
cases the mechanical factor is again responsible, while in others we 
have recently been convinced that biochemical reactions take place. 
Collis,? in his “ Milroy Lectures of 1915,” as well as the experimental in- 
vestigations of Mavrogordato,’ the statistical investigations of Brown- 
lee, Hoffman, and others, have shown that the most dangerous dust 
is that containing crystalline silica. The same is true to a certain degree 
of metallic dust, excepting perhaps iron dust. As to why coal dust, 
lime, plaster of Paris, etc., should be harmless in this regard, while 
flint, slate, tin, copper, etc., do promote the development of pulmonary 
tuberculosis, has not been explained satisfactorily. Experimental 
investigations of Mavrogordato tends to show that it mainly depends 
on the promptness with which various kinds of dust are eliminated 
from the lungs. It appears that dust entering the lungs excites an 
inflammation resulting in shedding of epithelial cells lining the air 


1 Ztschr. f. Aerztl. Fortbildung, 1918, 15, 39. 
2 Public Health, 1915, 28, 252, 292; 29, 54 
3’ Jour. of Hygiene, 1918, 17, 439. 


OCCUPATION 135 


passages. These cells pick up the dust and remove it promptly in 
cases of certain kinds of dust, as coal dust; while in the case of other 
kinds, as flint, or quartzite, this process of elimination is slow, or want- 
ing, and the foreign bodies remain within the lungs for months. Experi- 
menting with lamp black and pulverized glass, Corper! found that glass 
inhaled by guinea-pigs has a markedly accelerating influence, while 
lamp black has a retarding effect. 

Recent investigations have revealed another important point. It 
appears that the process is not entirely mechanical, but that bio- 
chemical phenomena play an even more important réle. It has been 
shown that dust inhalation is dangerous in proportion to the amount 
of quartz, or silica, it contains. But Haldane found that despite the 
fact that shale contains as much as 35 per cent of silicates (but not 
erystalline silica) it does not induce phthisis when inhaled for years by 
miners in England. Likewise, Brownlee found that the phthisis mor- 
talities among lead, iron, and coal miners reaches its maximum between 
the ages of fifty-five and sixty-five years, or ten years later than that 
found among silica workers, or males in general. With coal miners, 
among whom phthisis is a comparatively uncommon disease, it is at 
this age that the only approach to the level of the mortality among 
males in general is made. Among ironstone miners there is about 
twice the mortality of the coal miners at this age, and among lead 
miners about four times. He finds that while there is very little phthisis 
during early age among the general population, there is also very little 
among the miners, whereas, wherever early phthisis is common, it is 
also common among miners. On the other hand, Collis? points out 
that a form of tuberculosis with an age incidence conforming to Brown- 
lee’s middle-age type is extraordinarily prevalent among those who 
inhale dust of silica but not any other material. Those masons and 
quarrymen who work freestones suffer, but not those who work lime- 
stones; makers of silica suffer, but not makers of ordinary bricks; 
men who grind metal articles on sandstone wheels suffer, but not those 
who grind on carborundum or emery wheels; men who crush flint into 
fine flour suffer, but not those who crush emery or glass; miners who 
work mineral veins of tin, gold, or lead found in quartzite “country 
rock” suffer, but not those where country rock is of slate, or other 
non-silica material. 

In order to produce its deadly effect, silica must be present as uncom- 
bined SiO; if it exists as a silicate, e. g., in clays, the dust is not thus 
harmful. Collis suggests the following explanation why silica dust pre- 
disposes to lung disease: The chemical similarity between silica and 
carbon, as shown by their proximity in the periodic table, and their 
tendency to form colloid compounds may be the determining factor, 
permitting silica to replace carbon in the colloid complex of living 
protoplasm with the formation of new tissue, the tissue of the silicotic 


1 Am. Rev. Tubercul., 1919, 3, 605. 
2 Tubercle, 1920, 1, 54. 


136 PHTHISIOGENESIS 


nodule which, as Watkins-Pitchford has pointed out, is histologically 
so suggestive of fibrosarcomatous growth. Collis thus suspected that 
the process known as “silicosis” is effective in producing a definite 
chemical reaction in lung tissue which renders them a ready prey to 
the tubercle bacilli. 

More recent investigations by W. E. Gye! have confirmed the sus- 
picions that biochemical reactions are responsible for the development 
of tubercle. To begin with, Gye and Cramer found that the tetanus 
bacilli are pathogenic only when introduced into the body together 
with silica. If the soil in which the bacilli are carried does not contain 
soluble calcium salts of hydrated soluble silica, tetanus bacilli are 
harmless. They found that mice are sensitized to tetanus with silicic 
acid. Pursuing along the lines, Gye and Kettle have shown that silicic 
acid, and even silica dust, also sensitize these animals to tuberculosis, 
which spreads in the tissues injured by silica. That particles of silica 
disintegrate in the lungs into silicic acid has been shown by W. Watkins- 
Pitchford. 

These biochemical reactions are worthy of further study. They seem 
to open up a new field for investigations as to why, in most cases, 
tuberculous infection is more or less harmless, while in others it pro- 
duces deadly effects. But the field has hardly been scratched. 

Inhalation of Noxious Fumes.— Occupations involving the inhala- 
tion of noxious fumes have at various times been considered etiologi- 
‘ally related to tuberculous disease. Statistical evidence has not been 
in the direction of supporting this contention. But during the recent 
World War, when thousands of soldiers were attacked with various 
poisonous gases, it was found that while many of the survivors suffered 
from various pulmonary diseases, very few developed tuberculosis. 
Here we had an extensive experiment testing the etiological relationship 
of noxious gases to phthisis in human beings. Evidently it proved 
etiologically negative. Numerous cases seen by the writer, though 
showing symptoms and signs suggestive of tuberculous disease, have 
proved on careful and prolonged observation to be free from it. 

Social and Economic Conditions.—It thus appears from the brief 
survey of the subject that occupation per se cannot be considered as 
specifically predisposing to tuberculous disease, with the exception of 
those which involve exposure to, and inhalation of, metallic and certain 
kinds of mineral dust. But even in these occupations there are sig- 
nificant exceptions, as we saw in the case with street, iron, and coal 
dust, limestone, plaster of Paris, ete. 

There has, however, been found a correlation between the economic 
conditions of the workers and the incidence of tuberculosis among 
them. Economic conditions may be gauged by the wages paid to 
workmen. B.S. Warren,? in a study of conditions among the workers 
in the United States Government printing and engraving plants, found 


1 See Dale, Lancet, 1921, 2, 112. 
2 Tr. Nat. Tuberc. Assn., 1913, 9, 153. 


OCCUPATION 137 


‘that despite the fact that they are badly overcrowded, with poor ven- 
tilation, ete., the mortality from tuberculosis is rather low among the 
employees. He assigns as a reason the good wages paid by the Govern- 
ment to these workers. He finds from census statistics that low wages 
go hand-in-hand with high tuberculosis mortalities. The difference in 
wages or income means a difference in nutrition, social contentment, 
and general welfare, which renders the farm laborer more susceptible 
to phthisis than his employer, the cotton-mill operative more than the 
general population. Likewise, he finds that of deaths among males 
reported by the Census Bureau for 1909, giving the occupation of the 
deceased, 14.7 per cent were from tuberculosis, as against 20.9 per cent 
among females. The reasons for this disparity are many, but undoubt- 
edly the inadequate wages paid to women are responsible for a consid- 
erable portion of phthisis among female workers. The enormous 
increase of tuberculosis in European countries during and soon after 
the World War (see p. 89) points in the sam direction. Another 
fact in confirmation is the sharp increase in the morbidity and mortality 
from tuberculosis during the war in Europe, and its quick recession 
as soon as food has become more abundant. 


CHAPTER AY. 
PHTHISIOGENESIS. II. 


THE PHENOMENA OF IMMUNITY. 


Experimental Tuberculosis vs. Spontaneous Phthisis.—Infecting 
experimentally an animal with tubercle bacilli, we know exactly 
what morbid phenomena to expect. On injecting into the peritoneal 
cavity of a guinea-pig a certain quantity of the pure culture of tubercle 
bacilli, tuberculous peritonitis soon develops, followed by tuberculosis 
of other organs—the spleen, the liver, the lungs, the kidneys, etc., 
until it finally succumbs. But what will happen after a human being 
is infected in the usual spontaneous manner we cannot prognosticate 
with any degree of certainty. The individual may pass through life 
without showing any morbid manifestations which can be attributed 
to the infection. In fact, the vast majority of people have been infected 
during their childhood and are none the worse for their experience, 
as has already been shown. A large proportion of those in whom dis- 
tinct lesions of a tuberculous character have been found at the autopsy 
knew nothing about it during their life. On the other hand, in a certain, 
and it must be said a relatively small proportion, the infection is fol- 
lowed, sooner or later, by symptoms of some clinical form of tubercu- 
losis. 

This is, however, not the only difference between experimental 
tuberculosis and spontaneous phthisis as we meet it in human beings. 

It appears that phthisis is a disease met with exclusively in human 
beings and rarely, uf ever, in the lower animals; certainly not in animals 
which have been infected experimentally in the laboratory, be it by inocu- 
lation, ingestion or inhalation of tubercle bacilli. In guinea-pigs, rab- 
bits, etc., in whom spontaneous tuberculosis is exceedingly rare, only 
nodular tubercles, consisting of avascular, cellular masses, are formed 
after experimental infection; while spontaneous human phthisis is 
mainly a productive and exudative inflammatory process of the lungs 
in which there may, or may not, be any of the characteristic tuber- 
culous cell-proliferation. In other words, experimental infection in 
animals results in general or miliary tuberculosis, a disease but rarely 
met with in humans. “Real pulmonary tuberculosis,” says von Hanse- 
mann,' a pathologist of vast experience, “in the anatomical sense, is 
always part and parcel of general tuberculosis of all the organs in the 
body. Pure and isolated pulmonary tuberculosis in the anatomical 


1 Berl. klin. Wehnschr., 1911, 48, 1. 


THE PHENOMENA OF IMMUNITY 139 


sense, 2. €., in which there are no other tuberculous changes in the lungs 
than the development of submiliary tubercles, never occurs so far as 
my experience goes. But it is a noteworthy fact that from this disease, 
which in reality alone deserves the name pulmonary tuberculosis, 
phthisis never evolves. I know of no case in my own experience, nor 
from medical literature, in which the disease began as acute miliary 
tuberculosis in the anatomical sense, and then turned into pulmonary 
phthisis.”’ But phthisis may be, and quite often is, complicated by 
general miliary tuberculosis. This frequently occurs before the fatal 
termination of the case. 

In the same sense we find that Ribbert! makes a sharp distinction 
between experimental tuberculosis in animals, and phthisis in human 
beings: “It is undoubtedly a fact that tubercles may be produced in 
the lungs of animals which are made to inhale dust containing tubercle 
bacilli. But, (1) the disease thus produced is not the same as that 
in human beings; (2) we cannot, without further proof, conclude that 
human beings are infected in the same manner. The conditions under 
which humans inhale tubercle bacilli are, at least from the viewpoint 
of quantity, distinctly different from those prevailing during experi- 
mentation. It can neither be proved that individuals always inhaled 
tubercle bacilli before becoming sick, nor that the latter settled pri- 
marily in the particular organ in which they proliferated. Neither the 
clinical nor the anatomical findings sufficiently support this view. It 
is self-understood that I do not in the least deny that in man also 
disease may directly follow the inhalation of tubercle bacilli, but it is 
a question how often this takes place. From mere possibility to uncon- 
trovertible proof which will cover all tuberculous diseases of the lungs, 
is quite a distance.”’ “Pulmonary phthisis,’’ says Bacmeister,? “is a 
disease found exclusively in adult human beings; it never occurs spon- 
taneously in animals, nor has it ever been produced experimentally.” 

Before applying unequivocally experimental findings to man we 
must first demand that infection of animals should result in isolated 
apical lesions which extend gradually downward in the lung in the 
typical chronic manner. All other forms of tuberculosis which are 
produced experimentally in the lungs of animals do not prove much, 
because their morbid anatomy diverges considerably from the changes 
found in human phthisis. 

The problem why the human adult, after infection with tubercle 
bacilli, develops phthisis, a disease unknown in early childhood and 
among the lower animals, has not yet been solved to the satisfaction 
of all who are entitled to an opinion. Freund, Hart, Bacmeister, and 
others believe that pressure of a short rib or an ossified first costal 
cartilage upon the apex of the lung is responsible for the apical locali- 
zation of phthisis (see p. 118). We have, however, shown that this 
theory does not explain everything connected with the problem. 


1 Die Ausbreitung der Tuberkulose im Koérper, Marburg, 1900. 
2 Die Entstehung der menschlichen Lungenphthise, Berlin, 1914, p. 35. 


140 PHTHISIOGENESIS 


Various other theories have been promulgated to explain the origin 
of human phthisis. 

Intensity of the Infection.— After tubercle bacilli have sueceeded in 
gaining an entrance into the body, they cause disease only when the 
initial dose is sufficiently large and virulent, and they gain a foothold on 
susceptible tissues. Experience with most microbic diseases has shown 
that the average animal can withstand the entry of certain minimal 
doses without becoming sick with the specific disease. It is clear that 
in spontaneous infections we are not in a position to know the infecting 
dose. Experimentally it has been found that when the dose is small 
the animal may escape disease, though some authors report that very 
few germs, even one bacillus according to Romer, C. Fraenkel and E. 
Baumann,! may cause disease. Cobbett found that small doses of 
bovine bacilli, when injected into calves, produce only localized and 
limited lesions which soon become fibrous and calcareous, and thus 
assumed a retrogressive type; while the animals themselves, after 
transient disturbance of health, remained in excellent condition up to 
the time when they came to be slaughtered and examined. Medium 
doses (10 mg.), on the other hand, produced irregular results, while 
larger ones (50 mg.) invariably caused generalized tuberculosis which, 
in all but few animals (6 per cent), proved fatal within a few weeks or 
months (seventeen to seventy-six days). Gilbert and Gregg found it 
required between 10 and 120 bacilli to infect a guinea-pig. Webb and 
Gilbert found that this number of bacilli was sufficient to cause infec- 
tion, but not disease, in a human child. H. J. Corper showed that 
subcutaneous injection of 0.000001 mg. of moist culture produces 
tuberculosis in a guinea-pig within two months, while smaller doses 
usually produced only local lesions. Large doses produced multiple 
foci in various parts of the body. Employing a new method, Hugo 
Selter? recently found that one bacillus is enough to infect a guinea-pig 
by the subcutaneous and intravenous routes, and even by inhalation. 
When a larger dose is employed, it makes little difference as to the 
resulting disease, duration of life, etc., of the animal whether 100, or 
1000, 10,000 or 100,000 bacilli are used, provided that virus is injected 
intravenously, subcutaneously, or intraperitoneally. Thoeni and 
Thaysen,’ however, could not confirm these findings. They found that 
10 to 348 bacilli are insufficient to infect an animal when administered 
subcutaneously or intraperitoneally. They attribute the success of 
others to defective methods in counting the bacilli. 

Many writers have pointed out that there are significant differences 
in the result obtained in experimental infections according to the route 
by which the bacilli are brought into the body. Findel,* while exposing 
87 guinea-pigs to inhalation of tubercle bacilli, found that when a very 


1 Ztschr. f. Hygiene, 1906, p. 247. 
2 Veroffentl. Rob. Koch Stiftung, 1916, parts 11-12, p. 105. 
3 Zblit. f. Bakteriol., 1916, 77, 308. 
4 Ztschr. f. Hygiene, 1907, 57, 104. 


THE PHENOMENA OF IMMUNITY 141 


small number of the microérganisms, less than 50, were inhaled, disease 
results, and in young animals which are more susceptible than older 
ones, a single bacillus may produce a tuberculous lesion. On the other 
hand, enormous numbers of bacilli are necessary to produce infection 
by ingestion: Findel found that when 19,000 to 382,000 bacilli were 
given to 14 guinea-pigs with food, no tuberculous lesions could be dis- 
covered after cbserving them for as long as one hundred and seventy- 
four days. His experience has taught him that infection by ingestion 
can only be accomplished when the animal consumes at least 10 mg. of 
a pure culture of tubercle bacilli (about 35,000,000 bacilli). It thus 
appears that infection by ingestion is accomplished only when the 
infecting dose is about six million times greater than that required 
for infection by inhalation.. 

These interesting experimental findings cannot be applied without 
reservations to spontaneous human infection. These experiments were 
made with pure cultures of bacilli, and human beings hardly ever 
experience the entry of pure cultures by any route. Inhaled, ingested, 
or inoculated, the virus is always carried in dust, sputum, food, ete., 
together with various additional bacteria which may have an immense 
influence on the outcome. Moreover, we have seen that human beings 
display great resistance to tuberculous infection, even during infancy 
and childhood, and not all infections are followed by disease, and there 
are reasons to believe that only repeated infections with small doses 
of the virus, or a single very large one, is necessary to produce progres- 
sive tuberculous disease.! 

It would be rash to conclude that such large doses as would be 
necessary to infect experimentally an animal of the size of a human 
being are ever inhaled even in the proximity of a coughing consumptive; 
it appears that in most cases of such infections the dose is too small 
to produce disease. On the other hand, it is known that the bacilli 
multiply in the human body, and the few introduced, finding suitable 
conditions for life, may proliferate and produce disease of any magni- 
tude. Cobbett is inclined to attribute the harmlessness of small doses 
of bacilli to the following factors: After a minimal dose of bacilli 
enters the body, the organism at once begins to mobilize and develop 
its protective forces which are sufficient to deal with a few bacilli, while 
when a larger number is introduced, it may overwhelm the natural 
protective forces. This is confirmed to a certain degree by clinical 
observations in children. Most are infected with small doses of tubercle 
bacilli in early life, and are hardly harmed by the infection. A small 
proportion, particularly those subjected to massive infection, suecumb 
to acute tuberculous disease of some form. The mild infections enhance 
the work of the protective apparatus and prevent the multiplication 
of the bacteria; large doses can cope with the slight amounts of immu- 


1 For a complete review of the literature on this subject, see E. R. Baldwin and L. N. 
Gardner, Am. Review of Tubercul., 1921, 5, 429, 


142 PHTHISIOGENESIS 


nizing bodies which they provoke, and can keep on multiplying and 
destroy vital tissues. 

This may explain the immunity of children living in modern com- 
munities in which tubercle bacilli are ubiquitous. But it does not 
explain the development of phthisis in the adult who has been infected 
in early life with minimal doses of tubercle bacilli which remained 
latent for many years. The latter has been explained again by the 
various theories of predisposition, or diathesis, the innate, or inborn, 
tendency of some persons to acquire diseases which depends on certain 
peculiarities of the structure and function of the various organs of the 
body, all of which has been discussed in the preceding chapter. 

Phthisis Acquired during Childhood.—During recent years the 
theory that phthisis is a late manifestation of tuberculosis acquired 
during childhood has been gaining ground. Behring,! basing his 
opinions on experiments with guinea-pigs, maintains that a single 
infection cannot result in phthisis. He says that phthisis is the result 
of reinfection of a person who was already once infected during infancy, 
mainly through deglutition of milk derived from tuberculous cows. 
The bacilli pass through the gastro-intestinal tract into the lymphatics 
where they remain for years in an avirulent or mildly virulent state, 
and in the adult, as a result of some intercurrent affection, they become 
again virulent and cause phthisis. “ Phthisis is but the last verse of 
the song, the first verse of which was sung to the infant at its cradle.’ 

Hamburger’s*® conception of phthisis is also that it must not neces- 
sarily be preceded by recent infection, but that it is rather a reawaken- 
ing, or an exacerbation, of an old, “healed,” or latent tuberculous 
process. He points out that tuberculosis runs a different course in 
children from that in adults—pulmonary phthisis which is so frequent 
in adults is exceedingly rare in children. But we know that most people 
have passed through a tuberculous infection during childhood. Under 
the circumstances the inference is justified that pulmonary phthisis is 
invariably preceded by a tuberculous infection many years before its 
onset. 

To Hamburger the course of phthisis is similar to that of syphilis, 
with periods of health and quiescence, or latency, interrupted, or fol- 
lowed by periods of acute or subacute exacerbations. The primary 
lesion is inoculated during childhood, before the individual reaches his 
tenth year of life. During infancy this primary focus, if massive infec- 
tion has taken place, or the resistance is low, may cause miliary tuber- 
culosis, or hematogenous metastasis, but in the vast majority of people 
it heals, or remains dormant. In those in whom metastatic deposits of 
tubercle bacilli are distributed in various parts of the body, secondary 
tuberculous manifestations make their appearance, consisting in tuber- 


1 Deut. med. Wehnschr., 1903, 29, 689; British Med. Jour., 1903, 2, 993. 

2 Winfiihring in die Lehre von der Bekimpfung der Infektionskrankheiten, Berlin, 
1912; p. 354. 

3 Die Tuberkulose des Kindesalters, Leipzig, 1912, 


THE PHENOMENA OF IMMUNITY 143 


culosis of the glands, bones, joints, meninges, etc. After the tenth 
year the tertiary manifestations are met with, consisting in the various 
forms of chronic pulmonary phthisis, tuberculosis of the larynx, tumor 
albus, certain cases of joint diseases, of the kidneys, lupus vulgaris, 
tuberculous iritis, adhesive pleurisy, ete. These last are practically 
never seen in infancy and early childhood; only after the disease has 
lasted for many years they may appear, just as the late manifestations 
of syphilis—tabes, general paralysis, etc., are only rarely seen in early 
youth, although syphilis is quite frequent at that period of life. 

Phthisis is thus, according to Hamburger, an exacerbation of tuber- 
culosis which has been acquired during early childhood and remained 
latent for many years until some exciting cause, or a reduction in the 
powers of resistance, has brought about conditions favorable for its 
development. 

Latency of Tuberculous Lesions.—Before concluding that in the 
adult phthisis is an exacerbation of an infection with tubercle bacilli 
which has taken place during childhood, it must be ascertained whether 
living and virulent tubercle bacilli can remain within the body for many 
years without producing symptoms of disease. We have seen (Chapter 
III) that autopsy findings of persons who died from any cause, and 
tuberculin tests in the living have proved conclusively that 60 to 95 
per cent of human beings have tuberculous lesions in some parts of 
their bodies, and the majority remain healthy. We have also shown 
that the number of such latent lesions is very small during the first 
year of life, but increases annually, so that when reaching adolescence, 
the percentage harboring tuberculous lesions reaches over ninety. 

Animal experimentation has brought forward another important 
fact: Tubercle bacilli may remain for a long time in the tissues without 
producing gross, or even microscopical changes. Bartel, Weichselbaum, 
Macfadyen and MacConkey,! Goodale,? Rosenberger,* Harbitz,4 and 
others, have found this to be true in human beings. Bartel’ refers to 
this condition as the lymphoid latency of tuberculosis. He kept guinea- 
pigs in dwellings inhabited by consumptives, allowing them to roam 
around freely in the rooms and playing with the patients for several 
weeks. They were then kept under observation until their natural 
death, or killed when symptoms of disease were noted in them. At the 
autopsies it was found that of 27 animals, 17, though showing no gross 
pathological changes, had mesenteric and bronchial glands which were 
pathogenic when inoculated into animals. Similar observations have 
been made when human glands, removed surgically, or postmortem, 
were examined: No gross or even microscopic changes could be found, 
but when properly inoculated into animals, tuberculosis was produced; 


1 British Med. Jour., 1903, 2, 129. 

2 Boston Med. and Surg. Jour., 1906, 155, 632. 

3 Am. Jour. Med. Sci., 1905,°130, 95. 

4 Jour. Infect. Dis., 1905, 2, 143. 

5 Wien. klin. Wchnschr., 1905, 18, 218; 1906, 19, 25; 1907, 20, 1149. 


144 PHTHISIOGENESIS 


in some instances tubercle bacilli were even cultivated from such appar- 
ently healthy glands. As far back as 1890, Loomis found that in non- 
tuberculous persons 26.6 per cent were latent carriers of tubercle bacilli; 
Calmette! reports even higher percentages of tubercle bacilli in a 
latent stage, without any traces of pulmonary lesions in infants who 
died in hospitals for non-tuberculous patients, and who presented no 
symptoms of tuberculous disease, and he concludes that glandular 
infections have usually a tendency to remain latent. 

This lymphoid latency of tuberculosis may last for many years; 
in fact, for the natural life of the individual. But with advancing age, 
localization takes place and gross, as well as microscopic, changes of 
the affected structures takes place. Numerous lesions found in the 
glands, lungs, and pleuree of persons who died from other causes con- 
tain living and virulent tubercle bacilli, though during life no symptoms 
of this disease have been observed. This is observed not only in 
caseated lesions, but also in the fibroid, and even the calcified nodules 
found in adults. In other words, calcification of a tuberculous lesion 
does not kill the bacteria responsible for the pathological process. 
Investigations by Piéttre, Uhlenbrock, Rabinowitsch,? Lubarsch, Cal- 
mette, Guérin and Deléarde, and many others, showed that the chalky 
deposits found in the bronchial and mesenteric glands, in human beings 
as well as in animals, contain virulent tubercle bacilli. Calcified nodules 
are found mainly in adults, most commonly in persons over forty; 
they are hardly ever seen in infants under two years of age. While 
some of these nodules are completely surrounded by fibrous capsules, 
the majority are not, and at any time, when resistance is at a low ebb, 
the bacilli may invade the blood or lymph stream, and thus be carried 
to some vital organ where they proliferate and cause disease. While 
they may thus cause metastatic auto-infection, they ordinarily serve 
a good purpose in immunization, as we shall soon see. 

Considering the wide prevalence of this sort of tuberculous lesion, 
and that tubercle bacilli may remain in the tissues for years without 
causing any obvious anatomical changes, there is justification for the 
assumption of latent tuberculosis. For the clinician it is important 
to bear in mind that these latent lesions require no treatment, as a 
rule. When the equilibrium between the immunity conferred by these 
latent bacilli, on the one hand, and natural resistance of the carrier, 
on the other, is disturbed for any known or unknown reason, tuber- 
culous disease results from these bacilli. The form of the disease that 
may result from this metastatic auto-infection, or the organ that may 
be attacked, seems to depend more on the constitutional peculiarities 
of the patient than on the source of the virus. There are analogous 
conditions in pathology. The tertiary manifestations of syphilis are 
also caused by metastatic auto-infection from latent lesions; in malaria 
similar phenomena are observed. In leprosy a latency of twenty years 


1 L’infection bacilliare, Paris, 1920, p. 110. 
2 Berl. klin. Wehnschr., 1907, 44, 35; Ztschr, f, Tuberkul., 1910, 15, 217, 


THE PHENOMENA OF IMMUNITY 145 


and more after the infection is common. In fact, in this disease, there 
have been observed cases in which infection took place many years 
before the outbreak of the symptoms, and no chances for reinfection 
had been available during the long period of latency. 

Immunity or Allergy.—'The view of phthisiogenesis which has been 
gaining ground of late, and which apparently is based on a sound 
foundation, has been formulated by Paul Romer, to the effect that 
phthisis 1s a manifestation of immunity against tuberculosis which has 
been acquired by an infection during early childhood. 

It appears that the observations made in most of the transmissible 
diseases that one attack renders the individual immune against renewed 
infection with the same virus, hold good in tuberculosis; mild infections 
during childhood endow the organism with a certain amount of immunity 
against further and renewed exogenous infection with tubercle bacilli. An 
individual with a healed or latent lesion, acquired during early child- 
hood, is immune to these microdrganisms. Repeated infections with 
the same virus may be reinfection or superinfection. By superinfection 
is understood a second infection at a time when the lesions produced 
by the first infection have not healed, while reinfection implies a new 
infection when the lesions produced by the first have completely healed. 
“Tnasmuch as we may accept as a great probability that in tubercu- 
losis healing in the strict scientific sense never occurs,” says Ham- 
burger,! “all repeated infections in tuberculosis are to be considered 
superinfections.” We use the word reinfection because this term has 
gained extensive currency in medical literature. 

Experimental Proofs of Immunity.— Experimentally acquired immu- 
nity by an inoculation of tuberculosis has been proved to exist by the 
researches of Koch,? and then confirmed by Behring, Romer,® Hambur- 
ger, Webb and Williams,‘ Rossignol, Krause and Volk, Allen K. 
Kxrause,> and many others. When a healthy guinea-pig is inoculated 
with tubercle bacilli in pure culture, the wound closes within a couple 
of days and seemingly heals. But about ten to fourteen days later 
there appears at the site of the inoculation a hard nodule which soon 
breaks down, leaving an ulcer which presists until the animal dies. It 
is different when a tuberculous animal is inoculated with tubercle 
bacilli. The wound also heals, but no nodule is formed and a few days 
later the point of inoculation becomes indurated, dark in color all 
around the punctured point to about | cm. in diameter. During the 
next few days the spot becomes necrotic and the involved tissues are 
shed, leaving a flat ulcerated area which usually heals quickly, and 
permanently. Moreover, while after infecting a healthy animal the 
regional lymph glands become swollen, this does not occur after rein- 
fection of a tuberculous animal. 


Med. Klinik, 1915, 11, 34. 2 Deutsch. med. Wehnschr., 1891, 17, 101. 
Beitr. z. Klin. d. Tuberk., 1910, 17, 287; 1912, 22, 301, 

Jour. Med. Research, 1911, 24, 1. 

Am. Rev. Tubercul., 1919, 3, 1. 


10 


ao p oe 


146 PHTHISIOGENESIS 


The work of Rémer! and Hamburger? along these lines has modified 
our conception of tuberculous infection, and suggested prophylactic 
measures which are actually revolutionary. They have found that 
reinfection is as difficult and even as impossible in tuberculosis as in 
syphilis. All modes of infection were tried, inoculation, feeding, inhala- 
tion of tubercle bacilli in dust or spray, and contact infection, which 
are akin to the usual modes of spontaneous infection in human beings, 
but no new tuberculous lesion could be produced in tuberculous 
animals, while healthy controls were infected and succumbed to 
the disease in some form. Not only were guinea-pigs and rabbits— 
which are very susceptible—thus tried, but sheep which are not as 
vulnerable to tubercle bacilli, and also dogs which are strongly refrac- 
tory, and monkeys which display the same degree of susceptibility as 
man. Roémer found that when a healthy sheep is infected with a cer- 
tain dose of tubercle bacilli, it succumbs within eight weeks to acute 
pulmonary tuberculosis, but the same dose is harmless in a tuberculous 
sheep. In monkeys the results were the same. Hamburger and 
Toyofuko have proved that infected guinea-pigs are not only immune 
to inoculation, but also to inhalation, which is deadly to healthy con- 
trol animals. It appears from Rémer’s studies that this immunity is 
not transmitted by heredity, even when displayed by pregnant mothers. 

It has also been found that thisimmunity isnot only true of exogenous 
superinfection, or additional infection with bacilli of other strains, but 
also of superinfection with bacilli taken from their own lesions. 

Another important point was established by the experimental inves- 
tigations of Rémer and Hamburger: If the reinfecting dose of tubercle 
bacilli is small, perfect immunity is found—the point of inoculation 
heals quite soon. As a rule, the immunity is observed in animals which 
have been tuberculous for some time, three or four months. But if 
the reinfecting dose of tubercle bacilli is massive, it soon causes death 
of the animal. 

The results of these experimental researches are well founded, having* 
been confirmed by many workers in various countries, so that at present 
they are as firmly established as anything else we know about spon- 
taneous and experimental tuberculous infection. But there arise 
several problems of immense interest in our study of phthisiogenesis. 
Knowing well that the vast majority of human beings have been 
infected with tubercle bacilli during childhood, even those who have 
no clinical evidence of phthisis, we may justly ask, Can adults be 
infected with tuberculosis at all? The bearings of this problem on 
prophylaxis are enormous. How does phthisis develop from lesions 
acquired during infancy and childhood? Is it due to a second infection 
immediately before the onset of the disease, or do the old, hitherto 
dormant lesions for some reason flare up, begin to extend and produce 
metastasis ? 


1 Beitr. z. Klin. d. Tuberk., 1910, 17, 287, 383; 1912, 22, 265, 301. 
2 Ibid: 19LOsAG weal: 


THE PHENOMENA OF IMMUNITY 147 


Modes of Reinfection in Human Beings.—A person who has once 
been infected with tubercle bacilli may be reinfected with the germs 
which he harbors within the body, or with bacilli which have grown 
in the body of some other person, or in an animal. In the case of 
endogenous or autogenous reinfection the process may be very simple: 
A softened tuberculous lesion in the lung breaks into a bronchus, 
and during cough the tuberculous material is carried along the bronchial 
tree to some other part of the lung where it is deposited and, taking 
root, it produces a new lesion. In this manner there may also be pro- 
duced laryngeal and intestinal tuberculosis, the latter from swallowed 
sputum. But endogenous reinfection is not always bronchogenous; it 
may also be hematogenous—a tuberculous lesion may break into a 
bloodvessel and then bacilli are carried to various parts of the body; 
or it may be lymphogenous; the tuberculous material is carried by the 
lymphatics, infecting the lymph glands, etc. 

Exogenous reinfection should be very common, if it takes place at 
all. The bacilli are ubiquitous, and one suffering from any form of 
tuberculosis is evidently predisposed, otherwise he would have escaped 
the disease, despite the first infection. Infection is exceedingly easy, 
as is evident from the fact that when a child free from tuberculosis is 
brought in contact with a consumptive, it is soon infected. Hamburger 
even reports a case where exposure of an infant for one hour was 
effective in infecting it. We also see this to be a fact in adults: When 
individuals free from tuberculous infection dating back to childhood, 
as is the case with primitive peoples, come into contact with tubercu- 
lous people, they are soon infected, and succumb in a short time. 

Granting these premises, which are based on carefully observed facts, 
we may be able to study the problem of reinfection in man clinically, 
even though the experimental method is, for obvious reasons, closed 
to us. All we have to do is to inquire into the frequency of exogenous 
and endogenous superinfection and reinfection in tuberculous patients 
who are inmates in hospitals for consumptives; the frequency of tuber- 
culosis among those who are apparently healthy but live with consump- 
tives; and also the effects of tuberculous infection on persons who are 
known to have escaped infection during childhood. 

Reinfection in Hospitals for Consumptives.— Clinical experience has 
shown that it is extremely rare that a person should have one of the 
exanthemata twice during his life. It has also been observed that in 
a ward filled with cases of scarlet fever, smallpox, etc., there is no 
danger that patients suffering from the more malignant types of the 
disease should transmit the virus to those who are passing through a 
mild or abortive attack of the same disease. In nearly all contagious 
and infectious diseases we find that during the existence of the malady 
the patient is immune against exogenous reinfection with the virus of 
the same disease. The same is true of the exceedingly chronic trans- 
missible disease, syphilis. 

Experience in hospitals harboring large numbers of consumptives 


148 PHTHISIOGENESIS 


should give us information along these lines about tuberculosis. Here 
the patients have all the opportunities for superinfection with bacilli 
derived from other patients. For it must be agreed that despite the 
scrupulous cleanliness observed at present in sanatoriums and hospitals, 
it is impossible to avoid droplet infection when many patients are 
brought into intimate contact. In fact, caged guinea-pigs kept in 
scrupulously clean wards soon contract tuberculosis. 

It has, however, never been observed that a mildly infected patient 
or one in whom the disease has been “arrested,” living in an institution 
should be reinfected from one severely infected and in whom the disease 
is active and progressive, who shares the ward with him, even when 
the latter expectorates myriads of virulent bacilli, and offers excep- 
tional opportunities for droplet infection. 

Many non-tuberculous patients remain in sanatoriums for months, 
yet it has not been observed that one should become tuberculous 
because of his sojourn in the hospital. This is the reason why hospitals 
and sanatoriums do not separate the “open” from the “closed”’ cases, 
2. €., those who expectorate sputum containing tubercle bacilli from 
those who do not, in spite of the fact that many physicians are con- 
vinced that droplet infection is a potent factor in disseminating 
tuberculosis. 

The hospital staff, including physicians, especially laryngologists, 
nurses, orderlies, etc., come in close contact with the patients in sana- 
toriums and should become infected if adults, presumably infected 
during childhood, could be reinfected with tubercle bacilli. But, if the 
experience of thousands of people in these callings counts for anything, 
they do not show a higher mortality nor morbidity from tuberculosis 
than persons in other occupations. ‘The first statistics bearing on this 
problem were published by C. Theodore Williams,! who showed that 
long before the discovery of the tubercle bacillus, and before any 
precautions were taken to prevent the transmission of the disease, no 
case of infection of the hospital staff had been observed. From 1846, 
when the Brompton Hospital for Consumptives was opened in London, 
to 1882 “statistics showing that among the physicians, assistant 
physicians, hospital clerks, nurses and others, to the number of several 
hundred, who had served in the hopsital (not few of them having lived 
in it for a number of years continuously), phthisis had not been more 
common than it may be expected to be on the average among the civil 
population of the town.” In a later paper Williams? brought these 
statistics down to 1909 and found that conditions remained the same. 
But while during recent years the rarity of phthisis in the hospital 
staff, may be attributed to the improvement in the hygienic conditions, 
and the disinfection of sputum, this cannot be said to have been 
operative before 1882. During the thirty years of the existence of the 
Montefiore Hospital, no nurse, orderly, or physician has been observed 


1 British Med. Jour., 1882, p. 618. 
2 Ibid., 1909, 2, 433. 


THE PHENOMENA OF IMMUNITY 149 


to have been infected while attending to the needs of the tuberculous 
patients. The physicians who developed phthisis during the past ten 
years, have had histories of this disease before entering the service. 

Similar statistics are available for hospitals in Germany and France, 
published by Aufrecht,! Freymuth,? Brunon,* Saugman,‘ and others, 
and brought together by the author’ in a paper on hospital infection. 
Instructive data on the subject have been collected by Saugman from 
many sanatoriums in various countries. He finds that even among 
laryngologists, who are exposed to infection more than any other 
class, the morbidity and mortality from tuberculosis are less than 
would be expected. He concludes that tuberculosis is extremely rare 
among those who are engaged among consumptives; physicians and 
laryngologists who had been healthy before entering upon their duties, 
remain so. “It is not dangerous for healthy adults to be coughed at 
by patients suffering from pulmonary or laryngeal tuberculosis” con- 
cludes Saugman. 

Such facts have been quoted to disprove the transmissibility of 
tuberculosis, but in the light of our present knowledge they merely 
prove that reinfection is impossible. 

Marital Phthisis.— Bearing in mind the ease with which tubercu- 
losis is transmitted to persons who have not been infected previously, 
it is to be expected that the vast majority of husbands of tuberculous 
wives, or healthy wives of tuberculous husbands should acquire the 
disease. This, we know, is the case with syphilis, in which the active 
disease is almost invariably transmitted to the unaffected consort, 
excepting when the latter has been infected before marriage. But for 
a long time it has been a mystery why phthisis in both husband and 
wife is very rare in spite of the fact that they probably come into more 
intimate contact than even father and child. Even in families in 
which most or all of the children are affected with tuberculosis it is 
exceedingly rare to find that both the mother and the father should be 
sick with the disease. Formerly this fact was used as a strong argument 
against the transmissibility of tuberculosis, but now we understand 
that it is due to the immunity acquired by an infection which has not 
been effective in producing phthisis. 

For many years the writer’ was physician to a charitable society, 
having under his care annually 800 to 1000 consumptives who lived 
in poverty and in want, in overcrowded tenements, having all oppor- 
tunities to infect their consorts; in fact, most of the consumptives 
shared their beds with their healthy consorts. Still, very few cases 
were met in which tuberculosis was found in both the husband and the 
wife. Widows, whose husbands died from phthisis, were only rarely 

1 Munchen. med. Wehnschr., 1908, 45, 158. 
2 Beitr. z. Klin. d. Tuberk., 1911, 20, 231. 
5 La tuberculose pulmonaire, Paris, 1913, p. 59. 
4 Ztschr. f. Tuberk., 1905, 6, 125; 1907, 10, 224. 


5 Am. Med., 1915, 21, 607. 
6 Am. Jour. Med. Sci., 1917, 153, 395. 


150 PHTHISIOGENESIS 


seen to develop the disease. Among 170 couples in which one of the 
consorts was tuberculous, it wasfound that only in 2.5 percent were both 
the husband and wife phthisical; this notwithstanding the fact that a 
large majority lived very closely together, even sharing the bed. It 
has been my impression when investigating this problem that if under 
such conditions infection has not taken place, it cannot occur in any 
other adults. 

This experience is not unique. Mongour! found that among 440 
married couples, in which one of the consorts was sick with tubercu- 
losis, there were only 16 in which the partner was also phthisical, 7. e., 
4 per cent. Thom? reports 402 couples with only 12, or 3 per cent, in 
which infection of the consort had taken place in all probability. 
I. Burney Yeo? found marital phthisis comparatively rare, basing his 
deductions on particulars collected of 1055 cases of consumption. He 
cites figures of J. R. Bartlett, Herman Weber, and others and concludes: 
“Taking these figures for what they are worth, it seems certain that 
the communication of consumption from wife to husband, even among 
the class in which the conditions of life favor to the utmost the com- 
munication of contagious disease, is very rare; while it would seem 
that communication from husband to wife is more frequent.’ Pope,‘ 
Pearson, Elderton, and Goring have made careful statistical studies of 
this problem in England and arrive at the conclusion that the chances 
of tuberculosis occurring in both consorts are about the same as 
insanity, and a German writer has shown that cancer in both consorts 
is more apt to occur than phthisis. In a recent statistical study by 
Levy,’ comprising 315 married couples which lived in poverty, 34 per 
cent sharing the bed, possible marital infection could be traced only 
in 2.8 per cent. He points out that when marital phthisis does occur, 
it is characterized by a favorable course of the disease in the secondary 
cases, and soon after the actively diseased partner is removed, the 
infected consort recovers his or her health. Haupt found among 1553 
tuberculous couples that 106, or 7 per cent, were both affected. This 
being the highest percentage recorded, it is essential to remember that 
it is exactly the proportion in which humanity suffers from the disease. 

In this connection it is important to mention a curious phenomenon, 
first mentioned by Petruschky’ and which he named “mother immu- 
nity.’ A woman marrying a tuberculous husband begets children, 
most of whom either are sick with, or die from, tuberculosis, but she 
remains healthy. Gerald Webb® has observed the same condition, 

1 Cong. Intern. de la Tuberculose, Paris, 1905, 1, 413. 

2 Ztschr. f. Tuberkulose, 1905, 7, 12. 

3 British Med. Jour., June 17, 1882, p. 895. 

A Second Study of Statistics of Pulmonary Tuberculosis. Marital Infection, London, 
hy eee Heredity and Environment, London, 1912; The Fight against Tuber- 
culosis and the Death Rate from Phthisis, London, 1911. 

6 Beitr. z. Klin. d. Tuberk., 1914, 32, 147. 


7 Ergebnisse d. Immuntiitsforschung, 1914, 1, 189. 
8 Jour. of Laboratory and Clin. Med., 1916, 1. 


4 


THE PHENOMENA OF IMMUNITY 151 


though he is inclined to consider this as only a relative and not a com- 
plete immunity of the mothers, because they react to tuberculin, and 
he even found one of them to be herself a “carrier.”’ The present 
writer has had many women of this type under his care. Analogous 
conditions are seen in men, which may be called “father immunity.”’ 
A man marries a wife who dies from tuberculosis; he again marries and 
his second wife succumbs to the same disease. I know of one who had 
three wives die from tuberculosis, while he remained healthy. The 
children are usually tuberculous, or die from this disease. 

We have dwelt on these facts because they are very important points 
in phthisiogenesis: (1) Tuberculous infection can only occur once; 
and (2) phthisis develops only in persons who are, for one reason or 
another, constitutionally predisposed to the disease. Inasmuch as the 
non-phthisical consort has already been infected with tubercle bacilli 
during childhood, new opportunities for reinfection by cohabitation 
with a consumptive consort are of no avail to produce phthisis. It is 
his or her constitution that determines whether consumption will 
develop, and not the opportunities for reinfection. 

Clinical Evidence of Immunity Acquired by Tuberculous Infection. — 
Recent investigations have shown that a tuberculous bacteremia is 
not uncommon (see p. 284) in patients suffering from any of the 
forms of tuberculous disease, yet they do not manifest symptoms of 
acute miliary tuberculosis, as would be expected @ priort. Similar 
immunity phenomena have been observed in syphilis and malaria, 
and Morgenroth! has shown this to be the case in chronic jnfections 
with hemolytic streptococci. Whether it is a form of “depression 
immunity,” as Morgenroth suggests, or to some other cause, remains 
to be decided by further investigations, but there seems to be no doubt 
that mutual immunization of the parasite and host does occur in tuber- 
culous infection. 

A number of clinical facts, hitherto obscure, can be rationally 
explained by this acquired immunity of the tuberculous to the virus 
of tuberculosis, and they confirm the assumption that certain ex- 
perimental data obtained in animals hold good for man. Thus, 
despite the fact that so much sputum containing tubercle bacilli passes 
through the throat, mouth, lips, etc., tuberculosis of the mucous mem- 
branes and the cervical glands in adults is exceedingly rare. Patients 
with extensive tuberculous lesions of the lungs, expectorating myriads 
of tubercle bacilli, often have their teeth extracted or the tonsils 
removed by operation, yet no local tuberculous infection occurs, 
though tubercle-laden sputum surely remains on the open wounds. 

Scrofulous children have been noted by physicians for many genera- 
tions to display great resistance against the development of active 
tuberculous disease of the lungs in later life; many even speak of 
immunity. ‘The same is the case with other extrathoracie tuberculous 


1 Deutsch. med. Wehnschr., 1920, 46, 337. 


152 PHTHISIOGENESIS 


lesions. As will be shown later on (see Chapter XXX), persons with 
active tuberculosis of the glands, bones, joints, skin, ete., only rarely 
develop pulmonary phthisis. Mayo! points out that in Minnesota, 
where surgical tuberculosis is rife, phthisis is uncommon, and this has 
been observed to be the case in many other places. A large proportion 
of the population of Colorado is known to be descended from persons 
who emigrated to that State because of tuberculous disease. It has 
been observed, and recently confirmed by Whitney,’ that Coloradoans 
display a striking immunity against active tuberculosis. While the 
climate may be credited, still it does not explain this phenomenon 
completely. Natural selection, eliminating the susceptible stock, favors 
the propagation of those who have strong resistance. Their survival, 
despite the pathological stock, indicates that they possess unusual resist- 
ance, and that their descendants share in it. Clinical experience teaches 
that the prognosis in tuberculous patients is much better, and the course 
of the disease less stormy, in those who have descended from tuber- 
culous parentage, or who were “scrofulous ”’ during childhood (see 
Chapter XXX). 

The immunity of the tuberculous to tuberculosis is thus confirmed 
by a variety of clinical facts which can hardly be explained otherwise. 

Tuberculosis on ‘‘Virgin Soil’? in Human Beings.—In contrast with 
the immunity displayed by infected human beings against reinfection 
with tubercle bacilli, those free from the virus are very susceptible, 
and when infected the clinical phenomena are the same as those 
observed in experimental tuberculosis in animals. Bearing in mind 
that newborn infants are free from tuberculosis, no matter from what 
stock they are descended, it is suggestive along the lines of our inquiry 
that when infected, the resulting disease runs an acute and progressive 
course, Just as is the case in experimental tuberculosis in guinea-pigs 
and rabbits. For obvious reasons, no experiments of this kind have 
been made on infants. But there have been observed inoculations of 
tubercle in newborn infants among Jews when the wound made during 
ritual circumcision was infected by a tuberculous operator. The infant 
promptly becomes sick with tuberculosis, and the disease runs an acute 
and progressive course, the regional lymph glands being implicated. 
This is a drastic contrast to the mildness of tuberculous inoculation 
infections in adults, as is seen in the “butcher’s wart,” the “patholo- 
gist’s wart,” ete. Moreover, there are available certain observations 
which tend to show conclusively that adult human beings cannot be 
experimentally infected with tubercle bacilli. In February, 1900, 
Felix Klemperer* injected subcutaneously bovine bacilli into his own 
arm. ‘Ten months later he excised the indurated subcutaneous cellular 
tissue at the site of the injection and microscopic examination showed 
well-organized granulation tissue with giant cells, but no caseation. 

1 Jour. Am. Med. Assn., 1905, 44, 1156. 


2 Colorado Medicine, 1919, 16, 268. 
3 Ztschr. f. klin. Med., 1905, 56, 241. 


THE PHENOMENA OF IMMUNITY 153 


No tubercle bacilli could be discovered, showing that specific disease 
was probably absent, and the tissue changes were, at any rate, not 
characteristic of tuberculosis. Another physician, who had been tuber- 
culous for fourteen years, also submitted to similar injections of bovine 
bacilli. In this experiment the individual was given fourteen injections 
without producing any results. Four other tuberculous patients were 
injected with tuberculous lymphatic tissue from guinea-pigs. <A total 
number of thirty-nine injections of bovine bacilli were administered to 
these four patients. The local effects were slight. Four times abscesses 
were produced which, however, healed sooner or later. General con- 
stitutional effects were not observed in any case; the patients stated 
that they felt better, and they gained in weight during the experimental 
treatment. Klemperer concluded that, within certain limits, there 
appears no doubt that subcutaneous injections of bovine bacilli are 
harmless to tuberculous individuals. Baumgarten! performed similar 
experiments on cancerous patients with the same results. 

It is important to mention that experimental infections of physicians 
have, almost without exception, proved harmless. Thus, Alfred 
Moller? was infected intravenously with tubercle bacilli. He did not 
develop any acute disease, excepting that he lost in weight for a few 
months and then recuperated without showing any symptoms of tuber- 
culosis. Baldwin and Gardner also mention that Garnault injected 
virulent bovine bacilli into his own forearm with no harmful results. 
Ritter and Vehling® report accidental inhalation without harm of 
millions of dry, virulent tubercle bacilli by Hans Much and his co- 
workers. “It is difficult to avoid such accidents,” say Baldwin and 
Gardner,‘ “in research laboratories where dry material is manipulated, 
yet to our knowledge no authentic instance of their causing pulmonary 
tuberculosis has been reported.” 

Phthisis as a Manifestation of Immunity.— Irom the experimental 
and clinical data arrayed above, it is clear that neither infection with 
tubercle bacilli, nor predisposition, whatever this may consist in, is 
alone capable of producing tuberculous disease. To each one who 
becomes phthisical, there are many who have been infected with tuber- 
ele bacilli and remained healthy in the clinical sense. Indeed, spon- 
taneous infection acquired during childhood appears to render the 
body immune against further and renewed exogenous infection with 
the same virus. 

It is also clear that chronic phthisis occurs only in individuals who 
have been infected with tuberculosis during childhood, but have remained 
healthy until adolescence. In other words, phthists occurs only in persons 
who have been immunized by an earlier infection. In fact, it is in itself 
a manifestation of immunity, otherwise the patient would succumb to 


1 Berl. klin. Wehnschr., 1901, p. 894; 1905, p. 1329. 
2 Ztschr. f. Tuberk., 1904, 5, 211. 

3 Berl. klin. Wehnschr., 1909, 56, 1914. 

4 Am. Rey. Tubercul., 1921, 5, 436. 


154 PHTHISIOGENESIS 


acute general miliary tuberculosis, as do those who have not been 
immunized by earlier mild infection. This immunity is apparently 
sufficient to protect the individual under ordinary circumstances, 
but under certain conditions it may fail, and the person may be 
reinfected either from without, the tubercle bacilli being so ubiquitous 
that we can hardly escape them; or from within, by the proliferation 
of the bacilli that have been harbored in “healed” or quiescent foci, 
through metastasis. 

Acquired immunity in contagious diseases is hardly ever absolute— 
it is only relative, sufficient for the ordinary conditions of ife, and fail- 
ing during emergencies. The same appears to be true of the immunity 
acquired during childhood by infection with tubercle bacilli. It pro- 
tects the average person against exogenous reinfection with tubercle 
bacilli, and moderate failure of immunity permitting reinfection does 
not result in general tuberculosis, but only in phthisis—the most vul- 
nerable organ in the body, the lung, succumbs, while the others are 
still more or less protected. 

Immunity through Bovine Infection.—Some authors have been 
inclined to attribute the immunity observed in most adults to infection 
during childhood with the bovine type of bacilli which protects the 
individual against superinfection with bacilli of the human type. 
Clive Riviere! even advocates the immunization of humanity along 
these lines. He says that “until human sources of infection can be 
practically eliminated, or artificial immunization becomes an accom- 
plished fact, infection with the bovine bacillus through the use of a 
well-mixed milk remains our best ally in the campaign against tuber- 
culosis.”” We have seen already that bovine infection is fatal only in 
exceedingly rare instances. That it may protect against infection with 
the human type of bacillus is made highly probable by the rarity of 
phthisis in surgical tuberculosis. “Very significant in this respect also 
are the figures of McNeil for Edinburgh where, as shown by Fraser 
and Philip Mitchell, tuberculosis of bovine origin is particularly rife. 
Comparing Edinburgh with Vienna, he finds the incidence of tubercu- 
lous infection higher in the former for children up to the age of four 
years, and this in itself is highly suggestive of milk infection; but the 
valuable comment on this is the fact that the mortality from phthisis 
in Vienna is nearly three times as high as that for Edinburgh. Indeed, 
the high incidence of abdominal tuberculosis and the low mortality 
from phthisis are characteristic of Great Britain as a whole when com- 
pared with other civilized countries of Europe, and this may well bear 
the interpretation that it is the early bovine infection which protects 
against the inroads of pulmonary tuberculosis caused by the human 
strain of tubercle bacillus.’ Brownlee? also found that in England 
phthisis is less common in those districts in which there is a large 


1 British Jour. of Tuberc., 1914, 8, 83. 
2 An Investigation into the Epidemiology of Phthisis in Great Britain and Ireland, 
Part III, London, 1920, p. 55. 


THE PHENOMENA OF IMMUNITY 155 


number of deaths from tuberculosis in children, and also in the counties 
from which a large amount of milk infected with tubercle is sent to 
London. On the other hand, Bushnell! is inclined to think that chil- 
dren become immunized against infection with bovine bacilli, which 
they often ingest with milk, through previous contact with human 
tubercle bacilli. 

Failure of Immunity.— Obviously the evolution of phthisis does not 
depend alone on the intensity of the infection during childhood. The 
character of the soil: invaded by the bacilli is perhaps more important. 
Some succumb to hematogenous tuberculosis as a result of a mild in- 
fection, harmless to the average individual, which indicates that pre- 
disposition was a stronger factor. In what this predisposition consists 
we are in the dark, as has been shown in Chapter IV, in which most 
of the facts and fancies of this problem have been discussed in detail. 

Failure of immunity may be due to various complex biochemical 
changes in the body with which we are unacquainted at the present 
state of our knowledge. This is seen in children who have been infected 
but who thrive in spite of it, until an attack of measles, whooping-cough, 
ete., which is accompanied by a failure in allergy, as is evident from 
the negative outcome of the cutaneous tuberculin test during the active 
stage of the disease, flares up the latent tuberculous focus and tuber- 
culous bronchopneumonia results. Other febrile diseases may act in the 
same manner, but we do not as yet know the exact nature and effects 
of these biochemical changes in the body following contagious disease. 

The nature of predisposition is the stumbling-block of the theories 
of phthisiogenests. Clinical, demographic, and experimental observa- 
tions have not cleared up these important problems. It appears that 
no single predisposing factor, nor a combination of several factors, will 
fit most cases. As has been pointed out by Martius,? the predisposition 
of the individual is, after all, not a specific entity, which is possesed 
by those who are attacked by phthisis, and lacks in those who escape 
the disease despite infection. It appears to be a complex affair: In 
each individual case there are a number of anatomical and physio- 
logical factors which may each alone, or several in combination, decide, 
under certain conditions whether the person is to become phthisical 
and even these factors are subject to great oscillations, and may com- 
bine differently under different conditions. From this point of view 
everybody is predisposed to tuberculosis, but there are many important 
differences in the resisting powers of different individual persons which 
depend on the number, intensity, and accidental combinations of the 
various predisposing factors which, by themselves, are influenced by 
certain vital, biological oscillations occurring during the lifetime of 
the individual. We thus have gradations of predisposition from the 
strongest degree of vulnerability to the highest degree of immunity. 


1 Epidemiology of Tuberculosis, New York, 1920, p. 180. 
2 In Brauer, Schréder, and Blumenfeld’s Handbuch d. Tuberkulose, 1, 395. 


156 PHTHISIOGENESIS 


The various clinical forms of tuberculosis, acute, subacute, chronic, 
fibroid, ete., may thus be explained to a certain extent. 

Endogenous and Exogenous Reinfection.— Considering phthisis as a 
disease which develops only in an organism that has been immunized 
by an earlier infection which has left a latent or “healed” tuberculous 
focus in some part of the body, the problem arises whether the flaring 
up of the local lesion in the lung is caused by a new infection from 
without, by the invasion of new bacilli, or from within by metastatic 
migration of bacilli which have been kept dormant for years, until the 
immunity they conferred fails for some reason. 

Experimental findings on this point are somewhat conflicting. Orth 
and Rabinowitsch! have found that when guinea-pigs are infected 
with very small doses of mildly virulent tubercle bacilli which 
cause only local tuberculous changes, the effect produced is that a 
second infection with virulent human bacilli does not cause the usual 
generalized tuberculosis, but pulmonary tuberculosis results, bearing 
some analogy to pulmonary tuberculosis in human beings. In rabbits, 
which react to human bacilli in a manner similar to that of man more 
than guinea-pigs, they produced in this manner chronic tuberculous 
lesions in the lungs. Hamburger, Bartel, Levy, Hugo Selter, and others 
have confirmed these findings. This would indicate that phthisis is 
due to exogenous superinfection. 

That the outbreak of phthisis is due to autogenous, or metastatic, 
reinfection has been maintained by Behring, according to whom the 
primary infection takes place through the gastro-intestinal tract during 
childhood, the bacilli remaining latent until stirred into activity by some 
exciting cause. But if this were the case we should expect that pul- 
monary tuberculosis due to bovine bacilli would be very frequent, 
considering that at least 10 per cent of infections during childhood 
are caused by this type of microérganisms. As it is, there have been 
reported very few cases of phthisis in which the bovine bacillus was 
found exclusively. We have already mentioned that it has been sug- 
gested that those infected with bovine bacilli are immune against 
human bacilli, and they are the ones who escape phthisis despite 
tuberculous infection, but this would have to be proved. 

Romer and Much maintain that their investigations lead them to the 
conclusion that reinfection is always endogenous, or metastatic, from 
existing tuberculous foci within the body. “We know,” says Much,’ 
“that a tuberculous organism is not susceptible to, in fact it is immune 
against, superinfection from without. We must also admit that when 
an organism is infected during childhood it passes through a precarious 
crisis, but it may survive this first infection and remain endowed with 
immunity. But during adolescence, when great demands are made 
upon the vital forces, the body may be overwhelmed by the bacilli 
and the most vulnerable organ in the body—the lung—succumbs: 





1 Drei Vortriige iiber Tuberkulose, Berlin, 1913. 
2 In Brauer, Schréder, and Blumenfeld’s Handbuch d. Tuberkulose, 1, 247. 


THE PHENOMENA OF IMMUNITY 157 


thus phthisis results. One who hesitates in accepting these ideas of 
reinfection from within should only compare phthisis with syphilis.”’ 

There are analogous conditions known in pathology showing that 
an organism may harbor virulent bacilli without any harm to itself. 
Thus, the “carriers” of typhoid, diphtheria, meningococci, pneumo- 
cocci, and other bacilli may go around for years without showing any 
symptoms of disease, although they are a constant danger to others. 
But Texas fever illustrates this point even better. Cattle which survive 
an attack remain with the living virus within their bodies, but are 
immune against new infections, so that they may remain in infected 
pastures without any danger to themselves. But should they suffer 
from any secondary derangement, they may, as a result, experience 
an acute exacerbation of the process owing to sudden proliferation of 
the virus which has been dormant for a long time within their bodies. 

There are similar clinical phenomena in man. It is known that 
infection with the malarial parasite protects against further infection 
with the same parasite from external sources, and for this reason 
indigenous adult individuals in malarial districts are immune to 
malaria, as was shown by Koch. In some cases there occurs further 
infection in later years, and the result is a cachexia, a sort of malarial 
phthisis. But in such cases the initial infection must have been an 
especially strong and severe one. In syphilis this is even illustrated 
to better advantage. Superinfections are very difficult, usually 
impossible; the integuments and mucous membranes cease to react 
to the syphilitic virus introduced from without while they are sus- 
ceptible to their action from within. John A. Fordyce,! in a review 
of this subject, cites several other examples: “Levaditi has demon- 
strated that animals suffering with spirillary infection are immune 
to a new inoculation. Their serum has a high antibody content, 
but the blood still harbors parasites and is capable of producing a 
fresh infection in healthy animals. So with the serum of guinea-pigs 
inoculated with Nagana or Surra trypanosomes. This is trypanocidal 
for these organisms tn vitro, but in vivo they have acquired an insensi- 
bility to the trypanolytic antibodies, for the blood and tissues of the 
animals still contain parasites. The same is true of human subjects 
suffering from sleeping sickness in whose serum trypanolytic, agglutin- 
ating, and other protective bodies have been demonstrated. Carrying 
the analogy to syphilis we find that an individual may harbor spiro- 
chetes for forty to fifty years, while his skin and mucous membranes 
exhibit an insusceptibility to reinoculation under natural exposure. 
However, as soon as he is freed from his infection he is again in as 
susceptible a state as he was prior to his first attack.”’ 

We have shown that healed tuberculous lesions contain living and 
virulent tubercle bacilli; in fact, even calcified foci contain them. It 
has even been questioned whether once infected with tubercle bacilli, 


1 Am, Jour, Med, Sci., 1915, 149, 761. 


158 PHTHISIOGENESIS 


the virus is ever absent from the body. And for this reason we may look 
upon phthisis as produced by endogenous reinfection. Thus, according 
to Romer, phthisis is an acute or subacute exacerbation of a latent or 
quiescent lesion in the lungs acquired by massive infection during 
childhood, the bacilli remaining dormant for years, but when the 
immunity which they conferred failed, owing to some intercurrent 
disease, the lesion in the lungs flared up. That the specific immunity 
is not altogether lacking even under these circumstances is evident 
from the fact that the lesion remains localized for a long time in the 
most vulnerable of organs—the lungs. Phthisis is thus proof of 
immunity against tuberculosis. General miliary tuberculosis does not 
develop easily in the vast majority of individuals who have been im- 
munized by previous infections with tubercle bacilli. 

Immunity of Adults.—The question why adults are not immunized 
by mild primary infections, as children are, has not been explained 
satisfactorily. We have already mentioned that adults hailing from 
countries where tuberculosis is unknown, and where they could not 
have been infected during childhood because of the lack of tubercle 
bacilli, upon coming into cities, and in contact with tubercle-laden 
surroundings—subjected to primary tuberculous infection—soon suc- 
cumb to the acute forms of phthisis, like infants or guinea-pigs. Cob- 
bett! is inclined to attribute it to the cessation of the strain made upon 
the constitution by bodily growth. Be that as it may, he thinks that 
we may conclude that infection with tubercle bacilli, though it does 
not entirely cease when adult age is reached, is nevertheless, like infec- 
tion with most other diseases, less easily acquired then than in child- 
hood and adolescence. Much attempted to explain it by saying that 
either the organism of the child alone is capable of evolving a sufficient 
quantity of immune bodies, or we must assume that an adult person, 
coming from an environment free from tuberculosis to one which is 
tubercle-laden, freely going around among people among whom there 
are many bacilli carriers, is soon subjected to massive infection against 
which he does not possess sufficient powers of resistance. On the other 
hand, the sheltered infant does not roam around among various people 
during the first years of its life and comes in contact with only a few 
bacilli, so long as there is no active case of tuberculosis at home. 
I may add that the suggestion made above to the effect that the 
immunization of humanity during childhood may be accomplished by 
the bovine type of bacillus, which is not so virulent as the human type, 
may be responsible for this salutary condition. But this problem has 
not yet been worked out. 

Summary.—At the present state of our knowledge of tuberculous 
infection and immunity, particularly as regards chronic phthisis, the 
following conclusions appear justified: 

In civilized communities nearly all adults have been infected, though 
not all have acquired disease by virtue of this infection. 


1 Practitioner, 1918, 100, 404. 


THE PHENOMENA OF IMMUNITY 159 


Infection occurs in nearly all cases during childhood, the bacilli 
remaining latent within the body until some exciting cause reactivates 
them, or the natural resistance is reduced, and tuberculous disease 
results by endogenous reinfection. 

Infection during childhood, so long as it is not acute and fatal soon 
after the bacilli have entered the body, endows the organism with 
heightened resistance against renewed endogenous and exogenous infec- 
tion with tubercle bacilli. The immunity thus produced is, in most 
persons, ample to protect them against exogenous or endogenous 
reinfection with tubercle bacilli during the rest of life. 

When, for any reason, this immunity fails and the bacilli within 
the body are permitted to proliferate, metastatic reinfection may occur, 
new tuberculous foci develop, and clinical phenomena of tuberculous 
disease make their appearance. Experience tends to show that such 
metastatic reinfections mostly occur in individuals who were subjected 
to massive infections during childhood. 

Phthisis 1s thus a manifestation of immunity against exogenous and 
endogenous reinfection and superinfection with tubercle bacilli. When 
for any reason this immunity fails, no acute miliary tuberculosis 
develops, as is the case in massive primary infections, but only a local 
lesion results, the most vulnerable organ in the body—the lung— 
succumbs. 


CHAPTER VI. 
PATHOLOGY AND MORBID ANATOMY. 


THE TUBERCLE. 


TuBERCLE bacilli settling on susceptible soil offering suitable con- 
ditions for their growth induce a specific proliferation of the fixed 
elements of connective tissue, capillary endothelial, and probably also 
of the epithelial cells of the air vesicles, as well as an invasion of wan- 
dering cells. Acting as irritants, and injuring the cells and the inter- 
cellular substances, they induce a productive imflammation resulting 
in the formation ofa nodule, the specific granuloma termed tubercle 
by Laennec. 

This unit of the characteristic tuberculous process, the tubercle, 
is best studied in acute miliary tuberculosis, where tubercles of all 
ages—corresponding to successive invasions of bacilli into the blood- 
stream—are usually found. Throughout the lungs are scattered small, 
hard nodules. The younger ones are gray and translucent, the older, 
yellowish white and opaque. The transparent tubercles are smaller 
than millet seeds, while the opaque ones are larger, asarule. They are 
almost always larger and more numerous in the upper parts of the 
lungs where they grow better and more rapidly, which is perhaps corre- 
lated with the inferior blood supply of the upper lobes. Individual 
tubercles are too small to be seen clearly with the naked eye, and what 
we really see is for the most part fusions of several, conglomerate 
tubercles. 

Microscopically, the primitive tubercle presents a characteristic 
structure (Figs. 21, 22 and 23) of a fairly well-circumscribed conglomer- 
ation of cells. Primarily it is avascular; with the growth of the cells, 
the lymphatics and bloodvessels in its neighborhood are compressed and 
obliterated. In the typical young tubercle we see a multinuclear 
element called the giant cell, around which are cells which resemble 
epithelial cells in appearance and arrangement, and hence are called 
epithelioid cells (Fig. 23). At the periphery there is a stockade of 
lymphocytes. 

The Giant Cell.—The giant cell is most typically found near the 
center of the tubercle. But there may be several giant cells in a tubercle 
or, more rarely, there may be none. Exceptionally, particularly in 
conglomerate tubercles the giant cell or cells may be located toward 
the periphery. The giant cell is a multinuclear element with a stroma 
of fatty degenerated, or even necrotic protoplasm. It may contain 
as many as one hundred oval, spindle-shaped nuclei arranged concen- 





THE TUBERCLE 161 


trically like a crescent. The tubercle bacilli are mainly located in the 
giant cells (Fig. 22), where they may be seen singly or in clusters, 
usually at the inner side of the nuclei, or between the latter. They are, 
however, lacking in the center of the protoplasm of mature giant cells; 
probably the process of necrobiosis affects the bacilli as well as the body 
of the cell. In some tubercles the nuclei are located at the two poles 
(Langhaus’ type of giant cell), and occasionally there may be nuclei 
in the center. The cytoplasm in which the nuclei lay appears either 
quite homogeneous, or but faintly granular. Quite long streams of it 
can usually be traced between the neighboring epithelioid cells. In 





Fig. 21.—Microscopic tubercle. (Tendeloo.) 


thin sections, a fine network, the reticulum, is seen. The filaments are 
derived partly from extravasated fibrin, partly from curled fibrils of 
connective tissue, and partly from long, branching, interlacing processes 
of the cells, especially the giant cells, which have been described as 
looking like spider’s feet, and also from newly formed connective- 
tissue cells. 

The origin of the giant cells has been a debated subject. Some, like 
Weigert and Baumgarten, consider them the results of karyokinetic 
changes of the nuclei which retain the capacity for division, while 
the protoplasm, owing to the necrobiotic effect of the tubercle bacilli, 
does not divide into separate cells. In fact it is quite common to find 

11 


162 PATHOLOGY AND MORBID ANATOMY 


in tuberculous foci cells with degenerated protoplasm, while the nuclei 
show an increased chromatin content. From this point of view the 
giant cell is a degenerative phenomenon. On the other hand, Metch- 
nikoff sees in the giant cells a manifestation of phagocytosis. They 
are macrophages, or large active phagocytes, produced by the fusion 
of many epithelial cells with the object of fighting the invading enemy, 
the tubercle bacilli, with united forces. The part of the giant cell 
which has no nuclei is usually dead, because of the noxious effects of 
the tubercle bacilli. It is thus seen that the question whether the giant 
cells are derived from the fixed tissue elements (endothelial and con- 
nective-tissue cells, ete.), or result from the fusion of a number of cells, 





Fic. 22.—Tubercle, slightly enlarged, two giant cells in the center. (Ribbert.) 


or repeated division of cell nuclei without accompanying splitting of the 
cell body, has not been solved. If the latter is true, the division must 
be amitotic, for mitotic figures are not seen in the nuclei of the giant cell. 

Tubercle bacilli are mainly found in the giant cells, as has already 
been mentioned, and also in the epithelioid cells, while in the inter- 
cellular substance they are rarely noted. In the caseous parts of the 
tubercle, bacilli are found at the periphery, while they are never seen 
in the center. In the caseated giant cells they are found only in the 
parts which have retained their staining property. 

The Epithelioid Cells—The epithelioid cells are scanty in some 
tubercles, because they are composed mainly of lymphoid cells (lym- 
phoid tubercles), but more often the epithelioid cells predominate 


THE TUBERCLE 163 


(epithelioid tubercles). These cells are rounded, or somewhat elongated 
elements, whose cell body stains but palely in the ordinary hema- 
toxylin-eosin preparation, and is not very clearly outlined. The nucleus 
usually contains but little granular chromatin. As is the case with the 
giant cells, there is no unanimity as to the origin of these epithelioid 
cells. Maximow thought that they are derived from the lymphocytes. 
Baumgarten attributed them to the proliferation of the fixed tissue 
cells, while others see in them results of wandering cells coming from 
the blood stream. In a recent study of experimental tubercles, N. C. 
Foot! found confirmation of the suggestion that the epithelioid cells 
are derived from the vascular endothelium of the lesion. They, accord- 





Fic. 23.—Part of a tubercle very much enlarged; around the large multinuclear giant 
cell there are numerous epithelioid cells. (Ribbert.) 


ing to Foot, not only phagocyte tubercle bacilli, but carry them into 
the tissues, for example into lymph nodes by way of the lymphatics, or 
into other lung lobules by way of the air passages in which they are 
readily demonstrable. It is probable that the epithelioid cells may arise 
from the several varieties of fixed cells, depending on the location of 
the tubercle, such as capillary endothelium, ordinary connective-tissue 
cells, the Kupfer cells of the liver, the mesothelial lining cells of the 
serous sacs, ete. Still, it is possible that in some cases the epithelioid 
cells may arise from wandering cells. 

It has been demonstrated that the epithelioid and lymphoid cells 


1 Jour. Exper. Med., 1920, 32, 513, 533. 


164 PATHOLOGY AND MORBID ANATOMY 


lie in a fine reticulum which is partly, but apparently not wholly com- 
posed of fibrin. Also, here and there may be seen some remnants of 
the more resistant of the structures previously present, such as frag- 
ments of elastic tissue, ete. 

Histogenesis of the Tubercle.—The origin of the tubercle has been 
a debated subject for a long time, but the detailed studies of Baum- 
garten! have thrown much light on it. It has been noted that when 
tubercle bacilli are arrested in a small capillary, or on the wall of a 
terminal bronchiole, etc., the first reaction is not a dilatation of the 
neighboring vessels, exudation of numerous leukocytes, etc., as is the 
case in ordinary acute inflammatory processes, but rather the prolifera 
tion of the neighboring fixed tissue cells (endothelial cells, connective- 
tissue cells, etc.), which surround the bacilli. As was already stated 





Fic. 24.—Cross-section of tuberculous bronchus. The lumen of the bronchus is 
completely filled with muddy but quite homogeneous caseous matter and the mucous 
membrane has completely vanished. The rest of the bronchial wall is very rich in cells, 
and thickened. The thickening extends far into the neighboring alveoli. (Ribbert.) 


above, the proliferation of these fixed tissue cells results in the forma- 
tion of the epithelioid cells, and several of them may fuse around the 
bacilli to form a giant cell (in the formation of which cell division may 
also play an important part). Some of the cells are destroyed by the 
toxic action of the bacilli, and as a result some wandering cells are then 
attracted. At first these are the polynuclear, but these are soon 
replaced by lymphocytes, which form the peripheral part of the tubercle. 

Caseation.— The tuberculous follicles are therefore avascular neo- 
formations, and their vitality is not durable. No new bloodvessels are 
formed in them, as is the case with most other new growths. They 
are usually located in the alveolar framework, whence they compress 





1 Ztschr. f. klin. Med., 1884, 9, 93; 1885, 10, 24. 


PE Aaa | 


Fia. 1 





B, 





eee i 


Fig. I.—C, cavity in the pulmonary apex; F, interlobar fissure. To the 
left of the cavity are seen peribronchial nodules. Lower parts are exten- 
sively caseated. 

Fig. 2.—C, small caseous focus in the upper part of the apex; B, bronchus 
with caseated wall. The rest of the parenchyma is of normal air content, 
but anthracotie and showing black pigmentation. (Albert Fraenkel.) 





THE TUBERCLE 165 


the neighboring alveoli and finally obliterate them, and partly in the 
smallest lymph vessels, 7. e., along the walls of the smallest arterioles 
and bronchioles. In the arterioles a tuberculous obliterative endar- 
teritis is formed and this alone, or in conjunction with thrombotic 
phenomena, leads to occlusion of the vessel. In the small bronchioles 
caseous bronchitis may result, which may, however, arise primarily 
and lead to peribronchial tuberculosis secondarily. The bronchi 
become permanently plugged by their own secretions and by the 
irritative proliferation of their epithelium. The tuberculous growth 
finally compresses and destroys even the elastic fibers, so that in the 
center of the nodule there are only fragments of these tissues and often 
not even these, and air is completely excluded. 

The necrotic tissue is thus converted into a whitish or muddy, 
yellowish opaque mass; dry, often fragile, at times soft, or even viscous 
in consistency. It has the appearance of dry or soft cheese. Micro- 
scopically, the cells are found to have undergone fatty changes and 
ultimately death occurs by the process which Weigert called coagula- 
tion necrosis, the cells are converted into a structureless mass of detri- 
tus which refuses to stain. At times, we make out between the rem- 
nants of the cells a filament, consisting of a fine network of granular 
fibrin, or true hyaline fibrin, the so-called ‘‘fibrinoid reticulum.” 
Finally, a stage is reached when the débris of cells and fibrin become 
a homogeneously granular mass in which no structure is seen at all. 
This is true caseous matter.. ~ 

Some have suggested that tuberculous ‘toxins are specifically effec- 
tive in causing necrobiosis of the affected cells, but this has not been 
proved. It must be emphasized that desquamation of epithelial cells, 
necrosis, and caseation are not specific tuberculous changes. They 
are found also in various degrees of intensity in several other inflam- 
matory processes in the lungs. Necrosis, especially coagulation necro- 
sis, 1s also found in diphtheritic inflammation of mucous membrane, 
etc., and caseation in gummatous changes. The caseous gummatous 
nodule is often difficult to differentiate from the tuberculous. 

Calcification.— The caseous matter may become surrounded by a 
layer of connective tissue—encapsulated—and then, by the exclusion 
of water, it becomes inspissated and much reduced in size. In time 
small granules of calcium are gradually deposited until it becomes 
altogether calcified. Small calcified granules may coalesce into larger 
concretions, until finally they are converted into a dry, solid, jagged, 
or fragile concretion which looks very much like chalk. These concre- 
tions often contain virulent bacilli. In general, it can be stated that 
they are never dissolved or absorbed by autolysis, as is the case with 
other dead matter in the tissues. But caseous matter may be gradually 
permeated by fibrinous tissue and finally converted into a solid fibrous 
scar. 

Softening.— Very often the tubercle, instead of calcifying or under- 
going fibrosis, softens as a result of the action of proteolytic enzymes 


166 PATHOLOGY AND MORBID ANATOMY 


with which we are yet unacquainted. In this case there develops a 
puriform, thin liquid, without any pus cells but containing bits of 
cheesy matter, which is known as puriform liquefaction and ‘“tuber- 
culous pus.”’ In other cases real pus is formed, or a mixture of both 
liquids, which is also known as tuberculous pus. 

Sclerosis.—But the tubercle is not always destined to necrosis, 
caseous degeneration, calcification, or liquefaction. In most cases in 
which phthisis does not develop at all, or is checked in its progress 
and healing finally results, the nodule is converted into fibrous scar 
tissue through the agency of the proliferating connective-tissue cells. 
These connective-tissue cells are derived from two sources: [rom the 





Fia. 25—Indurated nodule in pulmonary tuberculosis. The solid nodule has a 
dark, caseous center with irregular lacune. It consists of coarse connective-tissue fibers 
in which carbon particles are deposited in some places. A giant cell is seen in the middle 
and to the right; three others are seen to the left. (Ribbert.) 


cells in the neighborhood of the tubercle, and from the tubercle itself. 
While making autopsies on persons who died from any cause patholo- 
gists have found that a large proportion have scars in their lungs and 
pleurse, thus showing that an enormous number of persons have had 
tuberculosis which healed spontaneously. These healed or dormant 
lesions are responsible for the large number of persons obviously non- 
tuberculous, yet responding to the tuberculin test. 

The fate of the tubercle depends on the intensity of the two processes 
of connective-tissue proliferation or sclerosis, and of caseation. In 
fact, the clinical course of the disease is mainly influenced by their 
relative intensity, the former being reparative, and the latter destruc- 


THE TUBERCLE 167 


tive. If the exudative process predominates and progresses with 
rapidity, the tuberculous focus increases in size and clinical signifi- 
cance; but when the proliferative process predominates, the inflam- 
mation proceeds slowly, and may even terminate in a cure through 
sclerosis. In chronic phthisis the two processes usually go hand-in- 
hand; the reparative, manifesting itself by the proliferation of con- 
nective-tissue cells, is seen at the periphery of the tubercle, while the 
center caseates. Pathologists then speak of fibrocaseous phthisis. In 
conglomerate tubercles the central foci may caseate, while those at 
the periphery are healing by sclerosis, and thus surround the lesion 
and prevent its progress by encapsulation of the cheesy center which 
finally calcifies, as was already shown. 

Tubercles in the Lung.—Gross Appearances.—In the vast majority 
of cases the tuberculous lung is found at autopsy to be adherent to 
the inner surface of the thoracic wall, at least the affected apex is found 
densely adherent. Very frequently the pleural sheets are so thick and 
dense that the lung cannot be removed from the thorax with ease, but 
must be torn forcibly, or cut away. In some cases the entire pleura is 
thick, and the pleural cavity is completely obliterated. The apical 
and diaphragmatic pleural sheets are, however, the parts most often 
thus affected. 

The external appearance of the affected lobe in chronic phthisis is 
irregular, deformed, or puckered, and of comparatively solid consist- 
ency. Frequently the surface of the lung is found studded with small 
pleural or subpleural tuberculous nodules; the interlobar fissure below 
the lobe in which the main lesion is located is usually obliterated by 
adhesions. The intrathoracic lymphatic glands, the hilus, mediastinal, 
and tracheobronchial are enlarged, hard and often dark because of 
anthracosis. On section these glands may be found in various stages 
of tuberculous degeneration, caseous, fibroid, or calcified. The first 
foci usually take root in the neighborhood of the apices and may 
remain there exclusively for a long time; in progressive cases, they 
extend by the production of new nodules. They usually consist in a 
combination of both productive inflammation in the form of nodule 
formation and a pneumonic process. ‘The first tubercles occur 
as single and isolated nodules, or groups, around the bronchi and 
the bronchioles, and at times also around the walls of the larger 
bronchi and the bloodvessels—peribronchial and perivascular tuber- 
cles. Varying with the intensity of the affection and the resistance of 
the individual, the nodules enlarge and extend slowly or rapidly and 
new ones appear around them. Large conglomerations of tubercles 
may thus beformed. In progressive cases the tubercles do not remain 
separated for a long time, but by fusion of many the focus enlarges 
and extends. The central nodules sooner or later begin to disintegrate 
and are converted into caseous matter. But in most cases a sclerotic 
process may be detected which limits its progress, excepting in the very 
acute types of the disease. 


168 PATHOLOGY AND MORBID ANATOMY 


On section the gross appearance of the typical tuberculous lesion in 
the lung presents a very variegated picture. In fact, there are hardly 
two cases which look alike. The scar tissue surrounding the cheesy 
centers, or insinuating itself within many caseous and softened areas, 
is a very strong substance made up of thick fibers and can be recog- 
nized by its color. It is dark because particles of carbon derived 
from the inspired air are deposited in it, and they cannot be expelled 
by expectoration because of their inability to reach the bronchial 
glands owing to the fact that the lymph channels are occluded or 
obliterated. It is therefore more or less dark gray, or even black in 
color, which contrasts distinctly with the various other colors of the 
lungs. The distribution of scar tissue is variable. In some cases it is 
mainly in the center of a group of tubercles, or it surrounds the caseated 
masses with extensive processes. A black, round or radiating scar may 
enclose a nodule the size of a pea or even larger, or several nodules. 
The cheesy matter is dry, and when old, calcified. This is very often 
found at the apex of clinically healed pulmonary tuberculosis. 

Later the caseous matter softens and, when the degenerative process 
extends, reaching and implicating the bronchial mucous membrane, 
the softened débris may break through the alveoli or the bronchi. 
But in most cases sclerosis prevents the spread of the lesion, and even 
encapsulates it with a more or less dense fibrous shell. Within the 
capsule the caseous matter dries up and finally calcifies, and it is stated 
that small foci may even be absorbed, though this is doubtful. 

There has been quite some discussion as to the origin of ulcerations 
on the surface of the bronchial mucous membrane and in the paren- 
chyma of the lung. Some have considered these as the points at which. 
the infecting bacilli have entered with the inspired air and set up 
the disease; that these ulcerations represent the primary tuberculous 
lesions. As far back as 1876 Parrot pointed out that in all cases of 
tracheobronchial adenitis such a primary lesion may be found in the 
lung if carefully searched for. This is known among French patholo- 
gists as la loi de Parrot, Parrot’s law. G. Kuss! has confirmed Parrot’s 
findings on extensive autopsy material, and more recently Anton 
Ghon? has found the same condition while doing numerous autopsies. 
French authors refer to these primary lesions as chancres tuberculeuz, 
and the enlarged regional glands which are almost invariably found, 
as bubons d’emblée. 

Others maintain that there are many cases of tracheobronchial 
adenopathy in which such a primary lesion in the bronchioles or 
pulmonary parenchyma cannot be discovered at the autopsy. It 
is also shown that even when found it should not be concluded in all 
cases that this ulceration represents the point of entry of the bacilli. 
It may be due to extension of the peribronchial nodules which, 
when enlarging, have reached the mucous membrane, caseated, and 


1 De hérédité parasitaire de la tuberculose humaine, Paris, 1898. 
2 Der primiire Lungenherd bei der Tuberkulose der Kinder, Berlin, 1912. 


« 


PLATE III 








wn ‘ 


ew 





i) ; 


Large Irregular Cavity with Shaggy Walls in Upper Lobe 
which is Covered with a Thick Pleura. 


Lower lobe shows conglomerative tubercles and gelatinous degeneration. 


, 


Anthracosis all over. 


PLATE IV 





Four Large Communicating Cavities, with Smooth, Glistening 
Walls and Crossed by Vascular Bridges. Pleura Very Much 
Thieckened. 


PLATE V 





Enormous Excavation of Nearly the Whole Lung. 


The wall is smooth, but traversed by thick bridges. Bronchial glands 
enlarged and ealcified. 


PEATE: Vi 





Caseous Pneumonia in Upper Lobe. 


Bronchi widely dilated. Miliary tubercles in lowerlobe. Enlarged bronchial 
glands, Pleura thick and covered with miliary tubercles. 


THE TUBERCLE 169 
produced ulceration. As was already stated in Chapter V, the problem 
whether phthisis is hematogenous or bronchogenous in origin rotates 
around this point, to a large extent. The experiments of Bacmeister 
have shown conclusively that such lesions may be produced by the 
hematogenous route, and that the primary lesion is not commonly in 
the mucous membrane. But this does not exclude infection of the 
mucous membrane. We have already shown that the bacilli may be 
deposited on the bronchial mucous membrane and pass through the 
lymph channels into the subepithelial tissue where they take root, 
without producing a lesion at the point of entry. 

Caseous Pneumonia.—The nodular formations are not the only 
changes wrought by the tubercle bacilli in the lungs. There are also 
seen larger primary infiltrations which are pneumonic in character; 
in fact, these distinguish phthisis from pure tuberculosis. These areas 
are of variable size, from that of a pea to that of an egg, or even larger. 
They are round, oval, leaf-shaped or lobular in arrangement; they may 
be single, or several may be found clustered together. They are pale, 
grayish and, later, muddy in color; at times they look like cheese. 
They are found in rapidly progressing fibrinous exudations which 
caseate quickly—caseous pneumonia. Real lobar caseous pneumonia 
is exceedingly rare. The diseased parts are voluminous, airless, heavy, 
like in the hepatization of lobar pneumonia. 

Microscopically, there is found an albuminous mass in which fibrin, 
red blood corpuscles and alveolar epithelium may be discovered, but 
the alveolar structure may still be made out at an early stage. When 
seen in the early stage we can follow the rapidly ensuing process of 
coagulation necrosis in the alveolar septe. Tubercle bacilli are found 
in large numbers, especially at the periphery of the cheesy focus. 
The final result is always the breaking down of the caseated and degen- 
erated débris, leaving excavations, which will be discussed later on, 
excepting when the process involves but a very small area, and some 
authors say that a cure is then possible by absorption of the caseous 
matter. 

Caseous pneumonia cannot always be differentiated from nodular 
tuberculous lesions, because when the nodules extend rapidly, as they 
do in some acute cases, they consist mainly of a conglomerate group 
of alveoli filled with exudate; the more rapidly the process progresses, 
the more they are coalescing and the greater the similarity to caseous 
pheumonia. 

Beitzke! points out the main differences between tubercle and case- 
ous pneumonia as follows: Caseous pneumonia is an exudative inflam- 
mation, while tubercle is a productive one. In the former there are 
therefore found loose exudate cells and fibrin, while in the latter solid 
tissue is found, and fibrin is almost never encountered. The exudate 
in caseous pneumonia lies in the lumen of the alveoli, while the tubercle 





1 In Aschoft’s Spez. pathol. Anatomie, Berlin, 1913, 2, 299. 


170 PATHOLOGY AND MORBID ANATOMY 


is located in the interstitial tissues. In caseous pneumonia the elastic 
fibers remain intact, while the granulation tissue of the tubercle 
destroys them. These differences show the necessity for differentia- 
tion between the two processes. But etiologically they cannot be sepa- 
rated: Both are due to the same cause, both combine and affect the 
lung tissue, so that only the microscope can decide the intensity with 
which each is represented in a given lesion. 

Localization and Fate of the First Lesion in the Lung.—The first 
lesion cannot be recognized at autopsies of cases of old chronic tuber- 
culosis, and it cannot be definitely determined whether the disease 
has arisen by the hematogenous or aérogenous route, as has already 
been mentioned. It appears, however, that the initial lesion heals in 
the vast majority of cases. It may also happen that the initial lesion 
should be completely, or partly, healed in one lung, while the second 
lung becomes affected with progressive disease. The nodules undergo 
complete fibrous replacement, become surrounded by connective-tissue 
which often implicates the surrounding overlying pleura, a cicatrix 
is formed which contracts the affected part of the lung, resulting in 
those puckered scars so often seen at autopsies. Inasmuch as the 
lymph channels are obliterated, the pigment particles inhaled with 
the inspired air cannot be removed, and they remain in the connective 
tissue, thus causing slaty induration. 

This mode of healing is not the rule. Often, though the focus caseates 
it is nevertheless surrounded by a fibrous capsule; the caseous center 
then softens, as has already been described. 

Extension of the Lesion.—The morbid focus may erode a blood- 
vessel and thus break into the circulation, causing acute general miliary 
tuberculosis, but this is comparatively rare, perhaps because of throm- 
bosis of the supplying vessels. Usually the process extends by the 
invasion of the tissues in the immediate neighborhood of the initial 
tubercle. Even when some sclerosis takes place, or the old tubercles 
calcify, the extension may proceed unabated. Conglomerate tubercles, 
massive infiltrations which are complicated by pneumonic processes, 
are thus evolved. 

The bacilli spread along the lymph spaces and lymph channels from 
the areas which have undergone pneumonic changes. ‘This is proved 
by the fact that around old lesions there is often found a crop of 
new tubercles. In the same manner occur fresh lesions in the neigh- 
borhood of old scars or calcified areas in the apex. Formerly it was 
thought that the latter are caused by new infections, or superinfec- 
tions, but since we have learned about the immunity of the tuberculous 
to new exogenous tuberculous infections, we consider these as metas- 
tatic endogenous extensions of the process. These metastatic tubercles 
increase in number, coalesce, and finally caseate. 

At times the extension of the process proceeds along the peribron- 
chial lymph channels and the result is a lobular arrangement of the 
focus, often looking like a mulberry. Some of these lesions, especially 


THE TUBERCLE 171 


when exudation takes place, simulate the bronchopneumonic picture 
very much. 

Metastatic extension of the process may also occur along the bron- 
chial tubes and then it runs a rather acute and progressive course. 
When a necrosed focus reaches the inner surface of a larger bronchus 
and breaks through the mucous membrane, the caseated matter is 
carried along the lumen of the tube and may be coughed out. But at 
times it is aspirated into the alveoli where it may produce a lesion 
of nodular type or a rapidly caseating pneumonic consolidation. Inas- 
much as in such cases we deal with larger numbers of bacilli, they may 
be distributed over larger areas. Most of these aspiration infections 
occur in the lower lobes of the lungs, but the metastatic infective matter 
may be carried to the apex by vigorous cough. ‘These metastatic auto- 
infections may produce disseminated tuberculosis, but in the majority 





Fie. 26.—Tuberculous cavity (a) at apex of lung, showing its relation to a bronchus. 
(Adami and McCrae.) 


of cases a single area is infected and the lesion extends by contiguity, 
or is of the caseous pneumonic variety; in others indurated nodules 
result. 

Dr. J. Kingston Fowler! has given in detail an account of the usual 
course of the secondary deposits in chronic or subacute phthisis as he 
found it while making numerous autopsies. He found that the first 
deposit of tubercles is not at the extreme apex. It is most commonly 
situated from an inch to an inch and a half below the summit of the 
lung and rather nearer to the posterior and external borders, and 
spreads backward, this line of extension explaining the fact that the 
physical signs of tubercle are often first noticed over the supraspinous 
fossa. In front, the lesions correspond to the supraclavicular fossa 


1 The Localization of the Lesions of Phthisis, London, 1888. 


172 PATHOLOGY AND MORBID ANATOMY 


or to a spot just below the center of the upper lobe, about three- 
quarters of an inch within its margin, and perhaps separated by an 
inch or more of healthy tissue. The second and less usual seat of the 
primary lesion is somewhat lower and more external, and corresponds 
to the first and second interspaces at the outer third of the clavicle. 
The lesion extends downward. The part which next shows tuberculous 
deposit is the apex of the lower lobe (the middle right lobe being passed 
over), from an inch to an inch and a half below the upper and posterior 





Fie. 27.—Wall of a pulmonary cavity. The upper part of the section shows tissue 
undergoing caseous degeneration, in which may be noted the following points: leuko- 
cytes whose nuclei have, at least in part, retained their staining properties; an obliter- 
ated vessel, some of the elastic tissue of which still persists; finally, a pulmonary arteriole 
almost blocked by endarteritis, the upper part of the vessel being included in the caseous 
coat of the cavity and in the process of tuberculous necrobiosis. (Letulle and Nattan- 
Larrier.) 


extremity, and about the same distance from the posterior border, 
a spot nearly corresponding to the chest wall opposite the fifth dorsal 
spine, midway between the scapular border and the spinous processes. 
This lesion tends to spread backward toward the posterior border of 
the lung, and laterally along the interlobar septum. The extension 
in the lower lobe is almost always from above downward and by 
islands of deposit of racemose shape with healthy lung between. The 
second lung is seldom the seat of secondary deposits until the lower 
lobe of the first lung attacked is implicated. The lesions are usually 


PEATE VII 





Voluminous Tuberculous Lung with Large Cavity Communicating 
with Main Bronehus. 


Bronehiectasis. Hilus glands enlarged. Lower lobe studded with miliary and 
softened tubereles. 








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_ a ah = 





THE TUBERCLE 173 


located in the same situations as those of the apex of the opposite side, 
but sometimes their site is close to the interlobar septum, midway 
between its upper and lower extremities, corresponding to the upper 
axillary fold. Extension in the lower lobe of the second lung follows 
the course of the lesions in the lower lobe of the first lung. 





Fia. 28.—Large subpleural pulmonary cavity. pl, thickened visceral pleura; p, sub- 
pleural pulmonary parenchyma transformed into fibrous tissue; f, groups of leukocytes 
accumulated under the visceral pleura; si, fibrous tissue under caseous masses which 
delimit the wall of the cavity; s, caseous masses formed at the expense of the pulmonary 
parenchyma and representing the zone of extension of the cavitary lesion; v, v, pulmonary 
vein placed in the center of projections which partition the cavity (remains of the inter- 
lobar framework); /, purulent masses loaded with bacilli attached to the surface of the 
cavity; a, pulmonary parenchyma not yet invaded by tuberculous caseation. (Letulle 
and Nattan-Larrier.) 


Cavitation.— When the caseated and softened detritus, affected by 
certain chemical changes, becomes undermined in various directions, 
blocks of dense tissue are loosened and cast off, then expectorated, 
leaving vacant areas in the lungs which communicate with one or more 
bronchi, ‘The walls may appear sinuous, pouchy and covered with 


174 PATHOLOGY AND MORBID ANATOMY 


caseous or purulent material and detritus of disintegrated tissues, or 
covered with a pyogenic membrane. In some cases they are smooth 
and glittering, all of which depends on their mode of origin. 

The excavations in phthisis may be single or multiple, and they are 
mostly located in the upper parts of the lungs, the apices. They may 
be the size of a hemp seed to that of a fist, and in rare cases the com- 
plete lung is excavated, leaving a thick shell of the pleura. William 
Ewart! pointed out that excavation is especially prone to attack defi- 
nite regions of the lungs. The apex of the lower lobe is thus affected 
at a date anterior to the implication of the lower parts of the upper 
lobe. The base and anterior border of the lower lobe are least prone 
to excavation, just as these parts are altogether the last to be involved 
in the tuberculous process. 

The question whether true bronchiectatic cavities may occur in 
phthisis has been debated. Ewart denied such a possibility, and when 
found, he considers it purely secondary to the undue strain thrown 
upon the spongy structures which escaped disease. But more recent 
investigations have shown that they may occur. Delafield and Prudden 
found them very frequently. The superficial layer of an affected 
bronchus may be cast off while the process of caseation goes on in the 
deeper layers. In fact, cavities may be formed without the destruc- 
tion of the inner bronchial lining. When the tuberculous process pro- 
ceeds slowly and proliferation of tissue is more active than necrosis, 
the bronchi dilate cylindrically and, because the more resisting ele- 
ments—cartilage and elastic fibers—perish, only an unsupported, 
smooth or slightly ulcerated mucous membrane remains, which yields 
to the expiratory pressure of the air during cough. These excavations 
are usually cylindrical or round in shape. They may be considered 
true bronchiectatic cavities. 

When multiple, the separating walls of cavities may be gradually 
destroyed and a sinuous vomica is thus formed. The large vessels and 
the affected bronchi resist the destructive process for a long time 
and remain as cylindrical trabecule, traversing the cavity in various 
directions. These tough septa and bridles are, however, not always 
remnants of persisting bronchi and bloodvessels. William Ewart has 
shown that they are more often chiefly composed of condensed airless 
lung, representing the remains of collapsed alveolar tissue originally 
separating discrete cavities. When finally these are also destroyed, 
only ridges and stumps of fibrous tissue remain within the cavity, 
and also septa which separate accessory excavations communicating 
with the main cavity. 

Only a small proportion of the cavities are bronchiectatic in origin; 
the vast majority arise through the hepatization and caseation of pul- 
monary parenchyma and expulsion of the necrotic tissue by expectora- 
tion. They have irregular, ragged walls on which there are attached 





1 British Med, Jour,, 1882. 


THE TUBERCLE 175 


pieces of necrotic tissue of various dimensions, bands separating rem- 
nants of interlobular septa of the lung. Within the cavity there are 
often found some large necrotic lumps of tissue, or sequestra, which are 
too large to be expelled through the communicating bronchus. On rare 
occasions a cavity is formed when a large part of caseated pulmonary 
parenchyma is sequestrated in toto. In case the cavity is derived 
from a small caseous peribronchial or bronchopneumonic focus, It is 
small, more or less circumscribed and round. But when it is derived 
from a larger pneumonic process it is large from the start and irregu- 
larly limited. But small excavations may fuse, coalesce, and form 
large, pouchy cavities. The septa which separate them fade away and 
a large, ragged excavation is formed; its walls are covered with a 
pyogenic membrane, consisting of granulation tissue and secreting 
tuberculous pus, like a chronic abscess. 

William Ewart thus describes the walls of tuberculous cavities 
which have been freed from secretions and débris: Internally the 
surface is lined with a grayish false membrane, often of appreciable 
thickness, but in other cases possessing a little more substance than 
the bloom of a fresh fruit. In either case it is readily detached and 
exposes a layer which constitutes the inner and vascular portion of the 
capsule, the outer portion of which is purely fibrous. The relative 
thickness of these three coats varies according to the age of the cavities 
and to the degree of irritation under which they may be placed. The 
chief features of tuberculous cavities are: (1) Absence of protecting 
epithelium; (2) gradual decay, leading to the formation of a necrotic 
layer (pseudomembrane); (3) gradual fibroid growth from without 
constituting the so-called capsule. 

Formerly it was stated that cavitation invariably implies mixed 
infection. T. Mitchell Prudden’s' experimental investigations have 
shown that injections of pure cultures of tubercle bacilli into the trachea 
of guinea-pigs and rabbits produced pulmonary infiltrations; when 
streptococci were added, cavitation was produced. But more recent 
investigations tend to show that tubercle bacilli alone are capable of 
producing excavations. In this country Ira Ayer? found cavities in 
the lungs of rabbits after injecting intratracheally massive doses of a 
suspension of tubercle bacilli containing many coarse clumps. Bac- 
meister’s experiments also showed that in animals in which tuberculous 
infection produces no cavitation, pressure on the apex will produce it, 
and that mixed infection is not necessary for the purpose. The pyo- 
genic microorganisms found in the walls and secretions of tuberculous 
cavities are now explained as secondary implantations of these organ- 
isms after cavitation has taken place as a result of the action of the 
tubercle bacilli. 

In slowly progressing or stationary cases a wall of connective 
tissue, even of non-tuberculous granulation tissue, may form around the 


1 New York Med. Jour., 1894, 60, 1. 
2 Jour. Med. Research, 1914, 25, 141, 


176 PATHOLOGY AND MORBID ANATOMY 


excavation, and the necrotic parts within are cast off and expectorated, 
leaving a smooth cavity. On the other hand, in progressive cases, 
the necrotic process digs itself deeper and deeper into the paren- 
chyma and the cavity keeps on enlarging and may attain extensive 
dimensions. With this process, non-tuberculous infection often takes 
place through the invasion of streptococci and staphylococci and other 
microodrganisms which invade the walls. Here mixed infection is 
frequently very effective in extending the diseased area. The pleural 
layers over superficially located cavities are usually united by dense 
adhesions. 

These cavities have a tendency to enlarge in the manner just 
described, but on rare occasions they may shrink because of vigorous 
sclerosis around the lesion which causes contraction. It is more 
common that the walls should remain smooth and quiescent for 
many years and, like a chronic abscess, discharge externally through 
a narrow sinus. But even caseous, ragged cavities may expel the 
necrotic tissue completely and permit the proliferation of connective 
tissue around the walls. Healing may thus result, the spongy con- 
dition of the adjacent lung favoring contraction. But such a course 
is less likely to occur when the excavation is extensive, owing to 
the surrounding caseous pneumonic processes which usually show a 
tendency to progressive decay. 

In extreme cases in which the excavations are extensive and the 
formation of connective tissue is vigorous, implicating the subpleural 
structures, the entire lung may be destroyed and reduced to the size 
of a man’s fist. In these cases the diaphragm is pulled upward and 
with it some of the abdominal viscera, especially the liver and stomach. 
The mediastinum is pulled over to the affected side, pushed along 
by the unaffected emphysematous lung. Complete dextrocardia may 
be found in such cases, with the tuberculous lesion in the right lung; 
in left-sided lesions the heart is often pulled to the left and upward. 

Closed Cavities.— Occasionally cavities are found in the pulmonary 
parenchyma which do not communicate directly with a bronchus, 
either because the lumen is occluded with the products of the exudate, 
or connective tissue has proliferated just at that point and plugged 
up the passage to the bronchus. Such a closed cavity may open up 
secondarily when the plug is removed from any cause. Perfectly closed 
cavities in the anatomical sense are not frequently encountered by 
pathologists, at any rate not so frequently as clinicians make such a 
diagnosis. 

Aneurysms of Rasmussen.—When the process of caseation and 
softening involves one of the bloodvessels, which very often traverse 
the walls of cavities, ulceration may extend to the vessel, causing pro- 
fuse and fatal hemorrhage. The walls of the exposed vessel become 
thinner and thinner and finally erode. Because of the loss of support 
due to the progressive inflammatory decay of the surrounding pul- 
monary parenchyma, it finally yields to the intra-arterial blood-pressure. 


PEACE Vill 





Acute Progressive Phthisis. 


Patient succumbed to a brisk pulmonary hemorrhage. Lung honey- 
combed with cavities; very large cavity in upper lobe. Most of the 
smaller cavities, as well as the communicating bronchus, are filled with 


clotted blood. Hilus glands enlarged and ecaseous. Pleura thiek and 
adherent. 





THE TUBERCLE 177 

More frequently hemorrhage occurs after the formation of an 
aneurysmal dilation of some branches of the pulmonary artery travers- 
ing the walls of the cavity (Fig. 29), first described by Rasmussen. 
The diseased arterial wall yields to the pressure, gives in first without 
rupturing owing to the withdrawal of support of the exposed side, 
and a sacculated aneurysm results; rarely a fusiform aneurysm results 
from the uniform dilation of the artery. Douglas Powell points out 
that the fibrotic cavities of old standing are more likely to develop 





Rea oe... 


Fic, 29.— Aneurysm of Rasmussen. The cavity is cut at two points and shows the 
wall (c) with a cavitary projection (a), the aneurysm, which is ruptured above. The 
blood has coagulated in the lower part of the aneurysmal sac. The wall of the cavity has 
a caseous lining which is continued into the aneurysm. Several pulmonary veins (p), 
included in the caseous lining, have been obliterated and can only be recognized by the 
remains of the elastic fibers. (Letulle and Nattan-Larrier.) 


aneurysm, and that aneurysm is more especially found on the exposed 
side of vessels which are partly buried in indurated tissue. It is diffi- 
cult to discern these aneurysms in most cases which come to autopsy 
because the cavities in which they are located are flooded with blood. 
Only after thoroughly washing the cavity may they be detected as 
white, round, sessile projections from the caseous wall of the excava- 
tion. They vary in size from that of a pinhead to that of a pea. 
Exceptionally they are of the size of a plum. They are usually single, 
but there may be found more than one and, in rare cases, more than 
12 


178 PATHOLOGY AND MORBID ANATOMY 


twenty have been found in one lung. In exceptional cases healed 
aneurysms of Rasmussen have been found in the tuberculous cavities. 

Because organized clots and thrombi obliterate the vessel, hemor- 
rhage is comparatively rare unless these aneurysms form. In small 
cavities the effused blood may by itself prevent further hemorrhage, 
providing the communicating bronchus is temporarily plugged, or is 
naturally of a narrow caliber. But many cavities are large and when a 
vessel ruptures, hemorrhage of great violence takes place. 

Rupture of a Cavity into the Pleura.— When a rapidly progressing 
excavation is located superficially in the lung and reaches the surface 
the pleura may caseate and rupture. In acute cases in which there 
is no time for the formation of adhesions between the pleural layers, 
a loss of continuity in the latter opens up a cavity and permits the 
escape of its contents, as well as air, into the pleural cavity. Pneumo- 
thorax is the result, and when this has lasted for some time, serous 
and purulent effusions—hydropneumothorax, pyopneumothorax, etc., 
are formed. These are quite rare in slowly progressing cases of phthisis 
because adhesive pleurisy results before rupture of an excavation 
takes place. In old cases I have observed that when pneumothorax 
does occur the rupture usually takes place into the pleura of the side 
that was only recently implicated. 

Reparative Processes.— We have already spoken of the process of 
repair that goes on hand-in-hand with the process of destruction in 
phthisis, and which is found to a certain degree in all cases excepting 
those of the most acute types. Judging by the large proportion of 
persons who at the autopsy are found with fibrous scars in the lungs 
and pleura, as well as with calcified foci in the parenchyma and glands, 
it becomes a convincing fact that more tuberculous lesions in the lungs 
are healed than progress to caseation and softening. It has also been 
found that many cases of these “healed” tubercles contain virulent 
tubercle bacilli and thus remain a constant source of danger: They 
may flare up at any time and again begin to progress, or by metastasis 
create new tuberculous foci in adjacent or distant parts of the lungs 
or other organs. 

Tendeloo! gives the following details about the reparative processes 
in pulmonary tuberculosis: 

1. Every fibrous focus is to be considered as an old tuberculous lesion. 

2. Calcification removes all danger of the further spread of the 
lesion. (This is not in agreement with the views expressed above and 
which are accepted by most authors.) 

3. A fibrous capsule separates quite effectively its caesous contents 
from the rest of the parenchyma of the lung, and the process may 
remain quiescent for a long time. So long as there remains caseous 
matter within the capsule, or non-fibrous tuberculous tissue, there is 
always danger that the caseous focus may extend beyond the fibrous 


1 In Brauer, Schroder, and Blumenfeld’s Handbuch der Tuberkulose, 1915, 1, 98. 


Lad 


THE TUBERCLE 179 


‘apsule, and also that the decay of the latter may favor a further exten- 
sion of the tuberculous process by growth and metastasis. So long as 
the bacilli remain virulent in the lesion, and there are connections 
between the contents of the focus and the surrounding pulmonary 
parenchyma through lymph spaces, they can grow under certain 
circumstances and induce pathological changes in other parts of the 
lung. On the other hand, a fibrous capsule interferes with medication 
reaching the lesion. 





Fia. 30.—Primary caseous focus in the left upper lobe with miliary tubercles in its 
vicinity. Caseation of the regional lymph nodes of the left upper lobe. Caseation of 
the upper tracheobronchial lymph nodes. Acute miliary tubercles in the lower tracheo- 
bronchial lymph nodes. Over both lungs disseminated tubercles are to be seen. The 
upper tracheobronchial and bronchopulmonary lymph nodes in the right side are free 
from pathological changes. (Anton Ghon.) 


4. A fibrous capsule has the same significance for an excavation. 
But in this case other dangers are added: So long as the cavities 
contain caseous matter, bronchogenous metastasis is threatening 
because there are always virulent bacilli in the caseous matter. The 
dangers of softening are greater in excavations communicating with 
the bronchi because the air has free access to their contents and may 
bring in other microérganisms, thus causing mixed infections. 


180 PATHOLOGY AND MORBID ANATOMY 


5. Healing of a cavity is possible when it is cleared of its contents 
and the walls granulate. Small vomice may heal when their contents 
are evacuated and the walls shrink. In more extensive excavations 
there always remains some vacant space. When no open lesion remains, 
the elastic fibers and bacilli disappear from the sputum. 

Jwart points out that whereas in other the organs the obliteration of 
abnormal spaces is effected by free granulations arising from the 
bottom of the cavity, surface granulations are practically absent 
from tuberculous excavations. Still, he holds that, if freely drained, 
they may granulate successfully and the walls finally adhere. This is 
in agreement with the more recent views of Tendeloo. But this is 
more likely to be seen in small vomice, while in the large ones the air 
and fluid contents offer obstacles to perfect contact of the surfaces. 

In general, we may consider the productive tissue changes as salu- 
tary, while the degenerative—caseation and softening—as phenomena 
lurking with dangers. Still, even in the latter healing is possible 
through calcification, or the removal of the products of tissue disinte- 
gration from the air passages. It is doubtful whether caseous matter 
‘an be absorbed, though some insist that this is possible. Exudative 
tuberculosis may terminate favorably or unfavoraby, according to 
its progress along the lines of absorption, or in other forms, caseation 
and softening, and elimination with the expectoration or by calcifi- 
‘ation. 

It-thus appears that even extensive tuberculosis may become quies- 
cent, although we cannot speak of healing and restitutio ad integrum 
in the anatomical sense. It must always be borne in mind in this 
connection that the anatomical changes are not the only ones which 
decide the outcome of the disease in most cases. 

Emphysema.— The unaffected parts of the lung in chronic phthisis 
often show emphysematous changes; in fact, occasionally on remoy- 
ing the lungs from the thorax after death, they may be found so 
voluminous that the tuberculous lesions is not seen without a search. 
The surface of the emphysematous parts of the lung is usually puck- 
ered because of the traction exerted by fibrous bands and excava- 
tions within the organ; or, in localized emphysema, which is more 
frequent, the surface shows bullse of various sizes. 

This emphysema is compensatory. When one lung is extensively 
involved by the tuberculous process, the other undergoes vicarious 
enlargement, at times encroaching beyond the middle line; when both 
lungs are affected, the unaffected parts become emphysematous. It 
appears that this is strictly for the purpose of enlarging the alveolar 
surface of the parts which remain intact thus increasing the breath- 
ing surface. In fact, microscopic examination of the emphysema- 
tous parts of the lung shows that there is no degenerative atrophy 
of the alveolar septa and bloodvessels, as in true emphysema. The 
alveoli are simply distended. 


PEAT ESA 





Liver Showing Amyloid and Fatty Degenerative 
Changes. 


“ 


THE LIGRARY 
OF THE | 


. 


: 


. 





THE TUBERCLE 181 


The Pleura.—The pleura is implicated in nearly every case of 
phthisis. A large proportion of cases are preceded by pleurisy, moist 
or dry, but even then it is usually secondary to extension of some small 
lesion in the lung. Pleural adhesions are found at the autopsy in nearly 
all fatal cases of phthisis, excepting those running an exceedingly acute 
course. In some cases they are so dense and compact that it is difficult 
or impossible to remove the lungs without injuring the pleura. Some- 
times the pleura is thickened all over; in many only partly, especially 
over the seat of the main lesions, and also at the base where thickening 
of the diaphragmatic pleura is not uncommon with resulting elevation 
of the diaphragm. Many fibrous bands are often seen extending from 
the pleura into the parenchyma of the lung. The adhesions may be 
lax and easily separated, but in many cases they are dense, and when 
extensive the thick pleura may surround the lung like a shell. In rare 
instances the pleura is even found calcified in places, or very extensively. 
Very frequently thickening of the pleura between the lobes of the lung 
is found. All these adhesions are great hindrances to the induction of 
artificial pneumothorax for therapeutic purposes. On the other hand, 
they prevent the occurrence of spontaneous pneumothorax through 
rupture of the visceral pleura over the site of superficially located 
pulmonary lesions, and when pneumothorax does occur, it is only 
localized. Serofibrinous pleurisy is quite frequent and, in fatal cases, 
exudation occurs in a large proportion shortly before death. 

The Larynx.—Primary tuberculosis of the larynx is exceedingly 
rare, but this organ is sooner or later affected in about one-third of all 
phthisical patients. While some of the lesions may occur as a result of 
inoculation by the sputum, it seems that the most common mode of 
access of the bacilli from pulmonary lesions is wa the lymphatics. 
This path of infection is plausible anatomically, and is supported by 
the fact that the earliest and predominating lesions are usually on 
the side of the larynx corresponding to the more extensive and active 
lesion in the lung. 

The process starts by the formation of multiple miliary nodules 
directly under the mucous membrane. These coalesce and undergo 
the usual fate of caseation and breaking down, with loss of substance 
and formation of irregularly outlined ulcers. Should the perichon- 
drium be reached, and it is in a large proportion of cases, necrosis 
of the cartilage results. While any part may be involved, the epiglottis, 
aryepiglottic folds, and true and false vocal cords are sites of pre- 
dilection. Occasionally, shallow ulcerations of the trachea result from 
inoculation by the sputum. 

The Intestines.— The intestines are only rarely the seat of primary 
tuberculosis. In children it has been found in between 30 and 50 per 
cent, and in adults Orth and Henke found it in 3 to 5 per cent of all 
autopsies. But in phthisis they are secondarily affected to the extent 
of 90 per cent of cases, according to some authors. Some of the 
anatomical changes are merely tuberculous nodules, but in most 


182 PATHOLOGY AND MORBID ANATOMY 


there are found ulcerations of the mucous membrane of the ileum and 
to a less extent of the jejunum and ascending colon (Tig. 30). These 
ulcers heal but rarely, though occasionally there is encountered a 
case of stricture of the intestine due to a contracted scar resulting 
from a tuberculous ulcer. On the other hand, these ulcers may per- 
forate into the peritoneal cavity with the usual results of these acci- 
dents. Ischiorectal abscesses are very frequent in phthisical patients. 

These ulcerations are not so closely restricted to the lymphoid 
nodules as those of typhoid, and they also differ from the latter by 
having their long diameter extending transversely to the direction of 
the gut, so that they are often known as girdle ulcers. Before the 
intestiné is opened the location of such an ulcer can be surmised by 
the linear arrangement of tubercles along the dilated lymphatics which 
are plainly visible through the serosa. The depth of the ulcers varies; 
they may extend down to the submucosa, muscularis or serosa, or they 
may perforate with the usual results of these accidents. Another form 











Fic. 31.—Tuberculous ulcerations of the intestines. (Tendeloo.) 


of intestinal tuberculosis—the so-called hyperplastic form—results in 
the formation of a mass of scar tissue in the neighborhood of the ileo- 
cecal valve, so that a large tumor is palpable, and symptoms of obstruc- 
tion result. 

The Peritoneum.— Pulmonary tuberculosis is also quite frequently 
complicated by tuberculous peritonitis. The bacilli may reach the 
peritoneum via the blood stream, or they may be deposited from a 
perforated intestinal ulcer, or a caseous mesenteric lymph gland, or 
a Fallopian tube. Depending on the number and mode of entrance of 
the bacilli, as well as on the resistance of the individual, the peritonitis 
may be localized or generalized. It may be almost purely plastic with 
the formation of dense adhesions, or there may be a large ascitic effu- 
sion. In some cases there are localized purulent effusions walled in by 
dense adhesions. Some authors believe that the localized thickenings 
of the capsules of the spleen and liver sometimes observed at autopsies 
are the results of a former tuberculous peritonitis. 


THE TUBERCLE 183 


Pathological Changes in other Organs.—It is exceedingly rare, if it 
ever occurs, for a case of pulmonary tuberculosis that leads to a fatal 
termination to run its course without implication of organs other than 
the lungs, pleura and larynx. Of course, all organs of the body will 
undergo, to a greater or lesser degree, the non-specific metabolic 
changes incidental to any long-standing toxemia, such as atrophy, fatty 
degeneration, ete. Moreover, the amyloid change that is prone in 
certain of the viscera during the course of chronic suppurations, is 
most frequently found in victims of tuberculosis, particularly of the 
bones and joints. 

But more important, perhaps, than any of the above-mentioned 
generalized, non-specific, nutritive disturbances are the specific lesions 
resulting from metastasis of tubercle bacilli to other organs of the body 





Fic. 32.—Miliary tubercles of the serous membrane of the mesentery of the intestine. 
(Ribbert.) 


. The bacilli may reach other organs from the lungs by the following 
routes: 

1. By direct extension of the pulmonary lesion, this being the usual 
mode of involvement of the pleura, as has already been shown. 

2. By transport of the bacilli with the sputum. Swallowed sputum 
is at times, though rarely, the cause of intestinal lesions. The common 
mode is, however, hematogenous and lymphogenous. 

3. By the lymphatics, this being the route of infection of the lymph 
glands draining the lungs. From the regional lymph glands of the lungs 
and intestines the bacilli may be very widely distributed via the lymph 
and blood streams. As has already been stated, the laryngeal lesions 
appear to result from lymphogenous transmission in most cases. 

4. Hematogenous transmission. ‘The presence of tubercle bacilli 
can very often be demonstrated in the blood of sufferers from pul- 


184 PATHOLOGY AND MORBID ANATOMY 


monary tuberculosis (see p. 284), and it is not surprising that hemato- 
genous metastasis in other organs occurs, particularly late in the disease. 
This appears to be the explanation of most cases of genito-urinary 
tuberculosis, tuberculous meningitis, and other distant visceral lesions. 

In this manner any organ of the body can be infected metastatically 
in the course of pulmonary tuberculosis, but some are much more fre- 
quently affected than others. 

The glands, especially those in the thorax—the bronchial, tracheal 
und mediastinal—and of the mesentery, are very often affected in 
children and adults who suffer from phthisis, more often than is gener- 
ally appreciated. In fact, it may be stated that the tracheobronchial 
glands are affected in nearly every case of phthisis. On careful and 
painstaking search small, microscopic tuberculous foci are often found 
in apparently unaffected glands; but the majority are swollen, enlarged 
and many are softened while others are calcified. In children these 
tuberculous glands very often give no clinical indication of their impli- 
cation; in fact, it is at times difficult to discover any changes in the 
bronchi and parenchyma on cursory examination at the autopsy. 
Still, these glands are frequently a source of trouble, not only in causing 
symptoms of tracheobronchial adenopathy, but also because these 
conditions are to be considered the forerunners of phthisis in the adult, 
though some look upon them as possible immunizing agents against 
reinfection in later life. 

By pressure these enlarged glands may cause stenosis of the main 
bronchus in children, while in adults it is less likely to occur because 
the bronchi are firmer. But the smaller bronchi may be compressed 
in adults as well as in children. In the latter, suppurating glands at 
times perforate the trachea, bronchi, pericardium, or esophagus, caus- 
ing sudden death, tuberculous bronchopneumonia, etc. 

The mesenteric glands are only rarely affected in adults, even in 
those who have tuberculous ulcerations of the intestines, but in 
children they are often found to be the seat of tuberculous changes, 
particularly with bacilli of the bovine type. This is in agreement 
with certain facts discussed in Chapter V. In primary infections the 
regional glands are invariably implicated. In secondary, or metastatic, 
infections the glands remain unaffected, as a rule. This rule holds good 
for the thoracic as well as for the abdominal glands. 

The Genito-urinary Organs.—The genito-urinary organs are quite 
frequently involved. Infection of the genito-urinary system secondary 
to pulmonary tuberculosis almost always takes its starting-point in 
either the kidney, or in the epididymis, or the Fallopian tubes, the other 
organs of reproduction and urination becoming implicated from these 
by extension or contiguity. These appear to be points of least resist- 
ance when hematogenous tuberculous infection is considered. 

Bones and Joints.—It is very uncommon that the bones or joints 
should become involved during the course of pulmonary tuberculosis, 
though in rare instances it is observed. The reverse is also true to 


THE TUBERCLE 185 


some extent: sufferers from osseous and articular tuberculosis rarely 
have active and progressive pulmonary lesions, excepting as a terminal 
phenomenon, when acute miliary tuberculosis, in which the lungs 
bear the brunt of the infection, may occur. 

The Muscles.—In fatal cases of tuberculosis the muscles are found 
pale or brown, atrophied and poor in fat; they appear to participate in 
the process of emaciation to an extreme degree. Microscopic examina- 
tion shows brown atrophy, fatty, and other degenerative changes. 
It appears that the diminution in the volume of the muscles is due to 
an atrophy of each individual muscle fiber, and not to diminution in 
their number. Tuberculous lesions are very rare in voluntary muscles, 
they being probably the part of the body most resistant to tuberculous 
changes. 

Nervous System.—While in rare instances the central nervous 
system proper contains tuberculous lesions, as large solitary tubercles 
of the brain, the most vulnerable part is the meninges, tuberculous 
meningitis being not an uncommon termination of pulmonary tuber- 
culosis. 

Circulatory System.—The circulatory system does not remain unaf- 
fected. The heart is small, weak, and atrophic, the individual muscle 
fibers being atrophied and fatty. Hypertrophy of the right heart may 
be seen in cases with extensive shrinkage of the lung with pleural and 
pleuropericardial adhesions. Verrucose endocarditis is seen in rare 
instances, but it is questionable whether this is due to the tubercle 
bacilli themselves, or to their toxins. The consensus of opinion is in 
favor of streptococci being the cause. In acute miliary tuberculosis 
miliary tubercles may be found in the myocardium, while in chronic 
phthisis they are rare. There have been reported some few cases of 
solitary tubercle of the myocardium. Pericarditis, often with copious 
effusion, is not uncommon. The bloodvessels also may suffer as a result 
of the infection. Tubercles in the walls of the arteries, veins or lymph 
vessels are not uncommonly found, and when they perforate the intima, 
they set up miliary tuberculosis. The pulmonary veins are the most 
frequent site of such tubercles. 

Amyloid Changes.—In those who have suffered from long-standing 
suppuration it is common to find deposited in the various organs a 
peculiar substance which Virchow termed amyloid from its supposed 
resemblance to starch and cellulose. Amyloidosis is particularly com- 
mon in tuberculosis of bones, though it is quite often seen in sufferers 
from pulmonary tuberculosis without osseous implication. 

While almost any organ may be involved, those most frequently 
affected are the spleen, liver, kidneys, and intestines. The spleen may 
be diffusely affected or, what is more common, the amyloid may be 
restricted to the Malpighian bodies (sago spleen). An affected liver 
may present no gross changes if the amyloid is slight in amount, or 
it may be very much enlarged and firm. The amyloid kidney is large 
and frm, the amyloid material being principally deposited within the 


186 PATHOLOGY AND MORBID ANATOMY 


glomerulus. The adrenals, lymph glands, intestines, etc., may also 
be involved. 

Amyloid possesses the property of staining a rich brown with a 
solution of iodine and potassium iodide. If strong sulphuric acid is 
used in addition to the iodine, the amyloid stains dark blue. With 
methyl violet, amyloid stains violet. Examination of histological prepa- 
rations shows that amyloid is never deposited in the cells, but always 
between them, being found in the walls of the small bloodvessels or 
just outside the endothelium of the capillaries. As it is deposited it is 
effective in causing pressure atrophy of the surrounding tissues; it 
also cuts off the blood supply by obliterating the capillaries. The 
chemical nature and origin of amyloid have been disputed. It has been 
shown to contain chondroitin-sulphuric. acid, and seems to be a com- 
bination of this substance with a protein fraction. 

In addition to the fatty changes of the heart, which have already 
been mentioned, the liver is frequently thus affected in pulmonary 
tuberculosis. The liver and spleen also often show frank tuberculous 
changes. KR. G. Torry! has reported 131 autopsies on tuberculous 
subjects at the Phipps Institute as regards macroscopic and 
microscopic changes in the liver, spleen, kidneys, ete. In the vast 
majority of cases that succumbed to pulmonary tuberculosis, tuber- 
culous changes were found in the above-mentioned visceral organs. 
O. Klotz? encountered tuberculous changes in the spleen, in 172 out of 
404 necropsies. A large proportion showed that the tuberculous lesions 
had healed. 


1 Am. Jour. Med. Sci., 1916, 151, 549. 
2 Tbid., 1917, 153, 786. 


CH Belo he Vek, 


SYMPTOMATOLOGY OF PHTHISIS—HISTORY OF THE 
PATIENT. 


We have seen that infection with tubercle bacilli does not inva- 
riably result in tuberculous disease. Phthisis implies a preéxisting 
infection, but the latter may take place without any subsequent clinical 
manifestation of disease. The diagnosis of tuberculous infection is a 
simple matter. The application of the cutaneous tuberculin test tells 
the story promptly, easily, and unequivocally. The chances of error 
are insignificant and may be disregarded. 

But a positive tuberculin reaction, found in over 90 per cent of 
humanity, as we have seen above, is by no means proof that the 
individual suffers from any disease, or needs general or special treat- 
ment. It only shows that the individual has been infected with tubercle 
bacilli at some period of his or her life. The infection may not have 
done any harm. In fact, we have seen that, in all probability, it has 
immunized him against a new massive infection, which is difficult to 
avoid, and which might have produced acute and progressive disease, 
had it taken root on virgin soil. 

“What we aim at in our practice is discovering not only tuberculous 
infection, but tuberculous disease. At any rate this is what the patient 
wants to find out: Whether he suffers as a result of the infection with 
tubercle bacilli, and whether any treatment is necessary to save or pro- 
long his life. This information can only be given after a careful and 
painstaking inquiry into the patient’s history, the symptoms he suffers 
from, and the physical signs elicited by an examination of his chest 
and other parts of his body, and applying some or all the clinical 
diagnostic methods which have been the achievement of medicine 
during the past couple of generations. 

Hazards of Hasty Diagnosis.— Realizing that the patient’s chances 
of recovery are greatest when the disease is recognized and treated at 
its very incipiency, there has been a strong tendency during recent 
years to treat every “suspect”’ as one who is actively tuberculous until 
time and observation prove the contrary. This advice has been given 
by many writers on the subject and followed by numerous physicians. 
As a result many innocent persons have been banished to sanatoriums, 
or to distant climatic resorts; many children have been deprived of an 
education, many workmen induced to leave their employment, many 
men of affairs to neglect their business. To be sure, some of these 
non-tuberculous individuals—“suspects’—have been fatigued and 


188 SYMPTOMATOLOGY OF PHTHISIS 


debilitated and needed a rest, and the error in diagnosis has rather 
benefited them. But with others things have been different. Many a 
person known to the writer has been trying to remove the stigma of 
tuberculosis, which he or she never had, without avail; and tubercu- 
losis is a stigma at present, despite our teachings that a patient who 
has common-sense and decency is as good, and as harmless, as any other 
person. 

We often meet with people who have spent some months in sana- 
toriums—from all indications they could have gotten along very well 
without it—and ever since they live in constant dread lest it will 
be found out that they had been “consumptives.” The stigma of 
sanatorium residence may later interfere with obtaining life insurance, 
with contracting a desirable marriage; at times even with obtaining 
lodging by those who have no blood relatives. In fact it may break 
up a family. I have known persons who have lost their jobs because 
some patient who knew them in an institution “gave them away.” 

A hasty diagnosis among the poor and moderately well-to-do—from 
which classes the bulk of phthisical patients are being recruited— 
works even more havoc at times. The results of the maxim, “Treat 
everyone as tuberculous until he proves to you that he is not,” can 
be seen in a city like New York where numerous individuals attend 
tuberculosis clinics for months, even for years, or go from one insti- 
tution to another for years, though they fail to present any reliable 
symptoms of active phthisis. I witnessed the autopsy on the body 
of a woman who remained twenty-six years continuously in an insti- 
tution; about one-half the time in a sanatorium, the other half in a 
hospital for advanced consumptives, where she finally died from 
pneumonia. Careful examination of the viscera failed to disclose an 
active tuberculous lesion. I calculated that the community spent, 
or wasted, over ten thousand dollars on this woman, not including 
the loss owing to her idleness. We may further mention that during 
the twenty-six years she kept out of the institution at least forty 
patients with active disease who might have benefited by the treatment. 

Many communities keep on spending considerable sums of money 
on the maintenance of patients who could be cared for in their homes 
at a lesser cost, or keep them from work merely because of a suspicion 
that they are tuberculous. Others break up their homes, commit their 
children to asylums because of a hasty diagnosis of incipient tuber- 
culosis based on some indefinite symptoms and physical signs. It was 
found in Germany, France, and England that some patients, passed 
for admission to sanatoriums because of incipient tuberculosis, were 
fit for active military service during the war. A large number of ex- 
sanatorium patients have been admitted to the United States Army 
and they made excellent soldiers. Fifty per cent of patients in one of 
our largest municipal sanatoriums have negative sputum; that this 
is an indication that many are non-tuberculous will be agreed to by 
everyone who has any experience with tuberculosis. With the anti- 


HAZARDS OF HASTY DIAGNOSIS 189 


formin method of sputum examination at most 10 per cent of active 
cases are found not expectorating bacilli. 

There appears to manifest itself a reaction against the eager chase 
for “incipient” cases which may swell the favorable statistics of 
sanatoriums. Authoritative writers now state emphatically that 
indefinite physical signs should not be relied on, and urge that only 
constitutional symptoms of toxemia be taken as criteria for active 
disease. Edward O. Otis! questions the wisdom of relying on ‘‘the 
presence of certain physical signs, definite or indefinite, with no 
symptoms of bacterial toxemia which are interpreted to mean active 
tuberculosis, and the patient exhibiting such signs is accordingly 
removed from his family and employment and consigned to a sana- 
torium, where there is at least some risk that he may receive a new 
and active infection. Whereas the individual was in no way ill, and 
probably never would have developed active clinical tuberculosis.”’ 

The harm done to the community by the principle of treating all 
“suspects” as tuberculous has been shown drastically during the World 
War. At first physicians examining soldiers thought that they were 
dealing with their civil patients and were hasty in making diagnoses 
of tuberculosis. In civil practice these would be admitted into sana- 
toriums where they would remain for a variable time, and be discharged 
as cured. But in the army, they were taken to hospitals for observa- 
tion and the result was that in France of 1000 such men, only 1.5 per 
cent were found to be actually sick with tuberculous disease, according 
to Kindberg and Delherm.2. About 113 of the men were merely troubled 
with chronic nose and throat conditions. Major Rist? stated that out 
of 1000 men in the French army sent back to a base hospital as suffering 
with pulmonary tuberculosis, 807 were found to be non-tuberculous. 
I have had under my care many who have either been rejected by the 
draft boards, or by disability boards, because of alleged tuberculosis 
which did not exist. The loss to the army in men and in money 
due to such hasty diagnoses cannot be overestimated. “The evils of 
such faulty diagnosis are world wide,” says Colonel G. E. Bushne'l;! 
“they have been encountered in the armies of Germany and of Great 
Britain, as well as in that of France. There is the same blame for us if 
we err on the side of a too minute and pedantic regard for slight changes 
in breath sounds, or in percussion, for all the world is committing, or 
until recently has committed, the same mistake, and the standpoint 
is maintained by so many writers of repute that the unwary are scarcely 
to blame if they believe that it represents the standpoint of the truth.” 
It is the opinion of Colonel Bushnell’ that “medical officers should be 
held strictly responsible for the exercise of enlightened judgment as to 
causes which may or may not be evacuated from their hospitals.” 


1 New Orleans Med. and Surg. Jour., 1914, 67, 311. 

2 Presse médicale, 1917, 25, 645. 3 Jour. Am. Med. Assn., 1917, 69, 1265. 
4 Medical Record, 1918, 92, 4. 

5 The Military Surgeon, April, 1918, 42, 383. 


190 SYMPTOMATOLOGY OF PHTHISIS 


A hasty diagnosis is as dangerous as neglect to recognize active and 
progressive disease. Delay does not mean sure death of the patient; if he 
is kept under careful observation, we cannot be too late making a positive 
diagnosis. The acute and progressive cases will manifest themselves 
very soon, and delay does not count because treatment in these cases 
is, as arule, not very effective. In the slow, sluggish cases the delay 
of a few weeks hardly ever makes any difference in the ultimate out- 
come. But pronouncing a patient phthisical when, in fact, he has no 
symptoms of active disease, is often followed by disastrous results to 
the patient as well as to those depending on him, and to the community 
which is charged with caring for its tuberculous dependents. It may be 
said without fear of meeting contradiction from competent sources that 
an incipient case in the full sense of the word does not always mean a 
curable case, or even a favorable case. Many cases justly classed as 
incipient have a worse prognosis than those considered “far advanced” 
in the conventional classification of the disease. 

Elementary Principles in the Diagnosis of Active Phthisis.— Active 
tuberculosis, or phthisis, manifests itself invariably by symptoms of 
bacterial intoxication. If there are no symptoms of constitutional toxemia, 
the patient may have been infected with tubercle bacilli—and who has not 
been?—but he is not sick with a disease which needs special treatment, 
costly to the community, and often ruinous to the patient and his family. 
Nor must the patient be isolated from his family, and hospitalized to 
prevent the dissemination of a disease which he does not have. This is 
a point which must always be borne in mind before a patient is told 
that he suffers from incipient phthisis. 

There is hardly a conscientious physician who is not skilled in making 
a diagnosis of incipient phthisis from the constitutional symptoms, 
even though he may have to leave the localization of the lesion to some 
virtuoso in physical diagnosis. There is no active phthisis without fever, 
cough, tachycardia, languor, night-sweats, hemoptysis, etc. Some or all of 
these symptoms are found soon after the patient becomes actively phthisical. 

If these elementary points were borne in mind by physicians, the 
number of mistakes of omission and commission would be reduced 
to a minimum. In fact, if the propaganda made so assiduously, 
aggressively and, within certain limits, justly, that to be cured, tuber- 
culosis must be discovered in its incipiency, would have insisted 
emphatically on the symptomatology of the disease, which can be 
inquired into, observed, and properly interpreted by every practising 
physician, all cases coming under the observation of physicians would 
be detected in proper time. It is wrong to blame the general practi- 
tioner for the large proportion of cases which are diagnosed rather late, 
after he has been taught that certain indefinite physical signs may mean 
phthisis, and just as often may mean nothing. In fact, the general 
practitioner may retort by saying that the large proportion of non- 
tuberculous cases admitted and kept in sanatoriums, as well as the large 
number of patients “cured” within two or three months in the insti- 


HISTORY OF THE PATIENT 191 


tutions, prove conclusively that the specialists are no less fallible in 
this regard. 

Natural Method of Arriving at a Diagnosis.— While in the practice 
of medicine we must often resort to the deductive method of reasoning 
when attempting to unravel an obscure case, yet in our attempts at 
ascertaining the presence or absence of active phthisis, we are on safer 
ground when applying the inductive method. We must first ascertain 
the individual symptoms and credit each with its true merit. In other 
words, all the morbid phenomena must be accurately observed; all the 
material facts are to be carefully inquired into; and, what is of most 
importance, the interpretation of the collected facts must be correct 
and in agreement as regards their relation one to another, and to the 
probable causes which may underlie the process. 

To do this rationally, we must carefully observe the appearance of 
the patient, go into details about the symptoms which urged him to 
seek medical advice and also inquire into such subjective symptoms 
as the average patient is not likely to note unless his attention is 
drawn to them. When all these data have been carefully gathered 
and properly evaluated, a physical examination is made to ascertain 
the objective signs of the disease, and these are correlated with the con- 
stitutional condition of the patient, with a view of ascertaining whether 
he is endowed with sufficient resistance to counteract the ravages of 
the disease. 

History of the Patient.— This is to be minutely inquired into. We 
find out the condition of health or the cause of death of the patient’s 
parents and grandparents, if he is in possession of the facts, or capable 
of giving them to us reliably, which unfortunately is only rarely the 
ease. Of particular importance is whether either of the parents was 
actively tuberculous when the patient was an infant. In case the 
parents have become actively tuberculous when the patient had 
already passed childhood, his chances of becoming phthisical are not 
greater than of those who do not have such an hereditary taint. In 
fact, there appears to be some evidence tending to show that, contrary 
to the general opinion, tuberculosis, if it occurs at all in such individ- 
uals, is apt to run a milder course than in those who have no family 
history of tuberculosis. 

We should not be greatly influenced by the age of the patient. No 
age is immune to the disease, but each age period appears to have its 
own form of the disease: In infants, hematogenous, general tubercu- 
losis is the rule; in children tuberculosis of the glands, especially the 
tracheobronchial group, the bones and joints; in adults chronic pul- 
monary tuberculosis; in persons over forty fibroid phthisis, and in 
aged individuals a very chronic form with a symptomatology and 
course peculiarly its own, etc. 

The occupation of the patient has great influence on the chances 
of developing active phthisis, as was already shown elsewhere (see 
p. 129), and should be considered when taking the history. A history of 
an injury to thechest, especially if followed by hemoptysis, is important. 


192 SYMPTOMATOLOGY OF PHTHISIS 


Preéxisting diseases are to be ascertained in detail. In infants and 
children active disease is apt to follow in the wake of one of the endemic 
contagious diseases; in adults, typhoid, influenza, pleurisy, pneumonia, 
diabetes, syphilis, ete., are of etiological moment; but their importance 
has often been overestimated by physicians. A history of scrofula dur- 
ing childhood has very little bearing upon active phthisis in the adult, 
excepting perhaps that if the disease does occur, it is likely to pursue 
a mild, and exceedingly chronic course. The same is true to a certain 
extent of previous tuberculous disease of the bones and joints. One 
has to consider the rarity of old scars on the neck or over joints of 
phthisical patients; or of active and progressive phthisis in those 
who have had Pott’s or hip-joint disease during childhood. (See 
Chapter X XX.) 

In women the menstrual history is to be gone into, and special 
attention paid to amenorrhea. It is also to be borne in mind that 
active symptoms very often appear immediately after childbirth. 
Here again it is to be emphasized that most women who suffer from 
active phthisis after gestation have had symptoms of this disease 
before conception and pregnancy. 

A history of exposure to infection should not be overestimated in adults, 
as has been advised by many writers. We have seen that those most 
exposed to infection with tubercle bacilli, as the hospital staffs of insti- 
tutions for the care of tuberculous patients—doctors, nurses, and order- 
lies—are not more liable to become phthisical than those in other walks 
of life who do not come into intimate contact with consumptives; nor 
do the unaffected consorts of tuberculous patients :suffer from this 
disease more than others. It is therefore absurd to expect that a tuber- 
culous fellow-workman is more likely to transmit the disease than a 
hospital patient to a doctor, nurse or the tuberculous to the unaffected 
consort. In my own practice I do not at all give exposure to infection 
any weight in the diagnosis of active phthisis in adults. It is different 
with children, especially with infants. Infants of tuberculous parent- 
age, or who have otherwise been exposed to infection, are very likely 
to have contracted the disease in an active form. With children over 
three we should ascertain whether the parent has become actively 
tuberculous while the child was less than one year old, because if the 
child was older than three years when the parent began to expectorate 
bacilli, the chances of primary massive infection of the child are remote. 

It is a curious fact that, in attempting to trace the source of infection 
in children, we often find it is one of the grandparents, suffering from 
senile phthisis, who is responsible, though he or she is ignorant of the 
true nature of the ailment, having been told that it is bronchitis, 
emphysema, asthma, ete. 

History of the Present Illness.—Of immense importance is the 
history of the mode of onset of the present ailment, as well as certain 
symptoms from which the patient has suffered during his lifetime. 
Previous attacks of “grippe,” “colds,” bronchitis, etc., may mean 


HISTORY OF THE PRESENT ILLNESS 193 


previous attacks of abortive phthisis and should be carefully considered. 
On the other hand, if we find that these “colds” are due to hypertro- 
phied tonsils, adenoids, etc., in other words, that they are manifesta- 
tions of the lymphatic diathesis, pulmonary tuberculosis in an active 
and progressive form is unlikely. Even if there is a distinct tubercu- 
culous lung lesion, the prognosis is very good. Previous attacks of 
typhoid fever, pneumonia, and particularly pleurisy, etc., may have 
been mild or severe attacks of unrecognized tuberculosis which have 
subsided. Having been treated for months for neurasthenia, gastritis, 
chlorosis, or even malaria, is not uncommonly ascertained in the 
history. 

We should inquire into the symptoms which ushered in the present 
ailment, with special reference to cough, expectoration, lassitude, 
languor, particularly in the afternoon, loss of weight, hemoptysis, 
pleuritic pains, or pleurisy with or without effusion, ete. Of most 
importance in ascertaining the presence or absence of active disease 
is fever with its concomitant symptoms—chills, backache, anorexia, 
tachycardia, etc. Night-sweats are to be inquired into and it should 
be ascertained whether they occur immediately upon going to bed, 
or wake the patient at some time during the night. The appetite of 
the patient is to be ascertained, and whether any loss in this direction 
has been concomitant with the appearance of other symptoms. If 
the patient knows, he should tell the fluctuations in his weight for 
the past several years. The condition of the bowels, especially the 
presence of diarrhea, is to be ascertained. 

Of course, if any sputum is available it should be examined micro- 
scopically for tubercle bacilli and elastic tissue. The urine should be 
analyzed for the presence or absence of albumin, sugar, and casts. 

After all these data have been ascertained, we proceed with the 
physical examination of the patient, and this includes not only a care- 
‘ful examination of the chest by inspection, palpation, percussion, and 
auscultation, but also all other parts of the body from the top of the 
head to the toes. We may thus find symptoms and signs confirming 
the diagnosis of phthisis, or proving that the symptoms of which 
the patient complains are due to some other cause. The stigmata 
of phthisis are often scattered all over the body, as will be shown 
later on. 

Above all, it must never be lost sight of that, while there is no active 
phthisis without constitutional symptoms, there is no single symptom 
or sign pathognomonic of the disease, excepting the expectoration of 
sputum containing tubercle bacilli, and even this is occasionally apt 
to mislead. It is only the combination and correlation of various symp- 
toms and signs which clinch the diagnosis, especially in obscure cases 
with negative sputum. This fact by no means interferes with the early 
recognition of active phthisis, and mistakes are more often due to 
carelessness in observation than to any other factor. 


13 


194 SYMPTOMATOLOGY OF PHTHISIS 


Importance of the Symptomatology of Phthisis.—In the succeeding 
chapters the physical diagnosis of phthisis in its various forms will 
be given its proper place, because only with the aid of inspection, per- 
cussion, and auscultation can we localize the lesion and gain impor- 
tant hints as to prognosis and the treatment indicated. The symp- 
tomatology of the disease, which has been given a subordinate place 
in some recent treatises on the subject, will be discussed in detail. 
The reasons are obvious: The general symptomatology of active 
phthisis can be ascertained by every practising physician, and its 
bearings on the presence or absence of active phthisis, especially in 
doubtful cases, are of more significance than indefinite physical signs. 
There may be active phthisis without physical signs revealing themselves 
even to the best-trained specialist, and even roentgenography may fail to 
disclose the site of the lesion, while many signs of apical involvement 
are found in healthy persons. But there is no active phthisis without 
constitutional symptoms. ‘This is an axiom which cannot be repeated 
too often. The symptomatology of phthisis, when properly studied and 
interpreted, gives information as to the onset of the disease, its activity, 
tendency, and ultimate outlook. It can be ascertained by any medical 
man. Inasmuch as it often precedes the appearance of definite physical 
signs, or the signs elicited with the aid of roentgenography, the symp- 
tomatology of the disease is to be ascertained first. 

We shall therefore begin with a discussion of the most prominent, 
and more or less constant, symptoms of active phthisis—cough, 
expectoration, fever, night-sweats, hemoptysis, anorexia, emaciation, 
tachycardia, etc. Each of these symptoms will be discussed from the 
standpoint of diagnosis, differential diagnosis, and prognosis. It is 
only by a proper appreciation of these symptoms that a diagnosis of 
active phthisis can be made at any stage of the disease, but especially 
in the so-called incipient stage; while a prognosis based only on findings 
during a physical examination and roentgenography is bound to 
prove disastrous to any practitioner in many cases. 





COlLUA Paley LUT. 
COUGH AND EXPECTORATION. 


COUGH. 


Frequency of Cough.—While cough is the symptom which first 
attracts the attention of the average patient to his troubles, there has 
been a question whether there are cases of phthisis without cough. 
Pidoux stated that cough is the first and last symptom of phthisis; 
when it is absent, its negative significance is almost absolute. Accord- 
ing to many writers, a patient who does not cough is not tuberculous, 
while there are others who consider it the most constant of symptoms 
of early phthisis. However, Louis, Wilson Fox, Moéller, and others, 
speak of patients who passed through the disease without ever coughing. 

This disagreement is due to various causes. The statement made by 
many phthisical patients to the effect that they do not cough is to be 
taken with considerable reservation. Mild cough, clearing the throat 
in the morning, or hawking, which eauses but little annoyance to 
individuals who are not given to introspection, may be overlooked. 
Even in the advanced stages, when considerable sputum is brought up, 
the patient may be under the impression that he does not cough— 
the sputum is carried by the cilia of the bronchial and tracheal mucous 
membranes, and when it reaches the vocal cords it is easily removed 
without effort, or swallowed. In the latter case the patient may not 
even expectorate. I have seen this to be the case with many patients, 
especially females. For this reason, it is often ascertained by close 
questioning that there is a little, mild cough, “just like everybody 
else coughs.” I have, however, seen many patients in whom physical 
exploration of the chest was negative for quite some time, but the 
continuous cough, productive or unproductive, was the only symptom 
which urged them to seek a diagnosis, and excited a careful study of 
the case by the physician. 

Another class of patients who do not cough despite active tuber- 
culosis are aged persons, of whom details will be given later on. The 
same is true of some cases of phthisis with cavities—mouthfuls of 
sputum may be brought up without any effort, or cough, as in bron- 
chiectasis. 

Cough in the Early Stage of Phthisis.—A considerable number of 
patients give a history of repeated “colds” caught during several 
preceding winters or autumns; or of attacks of “grippe’ which made 
them cough more or less violently, but they subsided under ordinary 
treatment. Owing to some neglect, the last attack has been per- 


196 COUGH AND EXPECTORATION 


sistent, the cough aggravated, and could not be relieved by the remedy 
which helped them formerly. The cough in these cases is apt to be 
rather mild, consisting mainly in clearing the throat in the morning, 
and may not at all be productive of sputum; or small lumps of clear 
vitreous secretion from the nasopharynx may be brought out. Rarely 
mucopurulent material is eliminated, but it is usually devoid of tubercle 
bacilli at this stage. In many cases the cough is due to irritation of 
the sensory nerve endings of the vagus within the bronchial mucous 
membrane by the secretion derived from the tuberculous lesion. 
Here tubercle bacilli are found, as a rule. 

These repeated attacks of “grippe,” or ‘“‘bronchitis,’’ which subside 
during the summer, to return during the autumn and winter, and are 
easily managed by ordinary sedatives, often give the patient a false 
sense of security, and when told that the cough is of tuberculous origin 
he is loath to agree to it. 

A careful examination of the throat is imperative in these cases. 
It must always be borne in mind that tuberculosis hardly ever begins 
with congestion of the rhinopharynx. When a cough can be rationally 
attributed to acute coryza or subacute rhinopharyngitis, and no signs 
are found while examining the chest, tuberculosis is only a very remote 
possibility. [ven in those who are undoubtedly tuberculous, the fact 
that they have hyperplasia of the glands of the throat, that they are 
“lymphatics,” points toward a mild, or even an abortive, course of 
the disease (see Chapter XXX). 

Mild cough is to be differentiated from hysterical cough, which 
is very frequent at present when phthisiophobia is rampant. In fact, 
in many homes with tuberculous patients, notably after a consumptive 
dies in the house, most of the healthy members of the family cough, 
believing they are affected with the disease. Perhaps the best sign is 
that hysterical cough does not occur at night, when the patient is asleep, 
or during the day, when he is absorbed in some matter which interests 
him. I have seen patients who coughed persistently, cease coughing 
during the time they were engaged in an interesting conversation. 
In many cases the cough in incipient phthisis is annoying at bedtime, 
disappearing during the first hours of sleep, and reappearing during the 
early morning hours, often waking the patient, while after rising it 
may be intense until the chest is cleared. During the day it may be 
scarce or absent and provoked only by emotional disturbance, undue 
exertion, chilling the body, a dusty or smoky atmosphere, ete. 

Paroxysmal Cough.—In many patients at the onset of the disease, 
or during its later stages, the cough is violent and paroxysmal; occurring 
in fits. When unproductive, it may be difficult to bear because it 
often increases in intensity during the evening, and keeps the patient 
awake during the night, causing pain in the chest, insomnia, and ex- 
haustion. In others, the fits keep up for quite some time until a small 
piece of viscid mucus is expelled. The first thing these patients ask 
for is a remedy which will loosen the sputum, During such spells 


COUGH 197 


vomiting may occur, or even involuntary evacuation of urine, espe- 
cially in women with lacerated genitals. These paroxysmal explosions 
of cough are a frequent cause of hernia in men, especially in those 
suffering from fibroid phthisis. 

Paroxysmal cough in phthisis is said to be due to ulceration of the 
trachea at its bifurcation. But it is also met with in cases of tracheo- 
bronchial adenopathy and adherent pleurisy. Its occurrence during 
periodical evacuation of pulmonary cavities will be discussed later on. 

Patients suffering from fibroid phthisis, and those who have tuber- 
culosis evolving in emphysematous lungs, suffer at times from severe 
paroxysms of cough. In these cyanosis of the lips and finger-tips, and 
bulging of the veins of the neck, are strong features during a paroxysm, 
and the suffering may be extreme. The violence of the cough is 
usually far out of proportion to the amount of sputum brought up. 
After the expulsion of a small lump of transparent mucus they feel 
relieved but exhausted, to be annoyed again at longer or shorter 
intervals. Nocturnal attacks are not uncommon. 

I have observed similar paroxysms of violent cough in many cases 
of galloping consumption in which the lesions could not be localized; 
also in miliary tuberculosis with tubercles widely disseminated all over 
the lungs, and signs of pulmonary emphysema were elicited on physical 
exploration of the chest. Some authors believe that the violence of 
the cough may be responsible for the extensive dissemination of the 
tubercles by metastasis. But in many cases under my care the lesion 
finally localized itself, and the disease pursued the usual course of 
chronic phthisis, the paroxysmal cough disappearing, leaving the com- 
mon cough encountered in the average case of the disease. 

The Emetic Cough.— First described by Richard Morton at the end 
of the seventeenth century, the cough ending in vomiting, is quite 
frequently met with in the early stages of phthisis in various degrees 
of intensity. Some French authors, notably Paillard,! state that the 
signe de Morton, or the toux émétisante, as they call it, is met with to 
the extent of 50 to 60 per cent of all cases of phthisis. This has not 
been the case with the patients under my care. ‘To be sure, vomiting 
may be seen in more than one-half the cases of tuberculosis at some 
period of the course of the disease, but not all vomiting can be con- 
sidered the true emetic cough, as we shall soon show. 

It has been stated that the cough of incipient phthisis often produces 
no expectoration, but vomiting. There are tuberculous patients who 
cough as soon as they eat, says Michel Peter,? there are others who 
cough because they eat; finally, there are others who, having eaten, 
cough, vomit, and suffer from cardiac palpitation. This emetic eough 
ws so characteristic that when whooping-cough and rhinopharyngitis in 
chronic alcoholics are ruled out, I place great reliance on it in doubtful 
cases, and it has often helped me in making a positive diagnosis sooner 


1 La toux émétisante des tuberculeux, Paris, 1911. 
2 Legons de Clinique médicale, Paris, 1879, 2, 318. 


198 COUGH AND EXPECTORATION 


than I could have made it without this symptom. But to appreciate 
its diagnostic significance it must not be confounded with vomiting of 
other origin which may occur in phthisis. It usually occurs in the 
following manner: 

The patient has had his lunch, or dinner, with a variable appetite 
and feels rather satisfied, having no sensation of gastric disturbance, 
excepting perhaps some feeling of epigastric distention or mild dyspnea. 
But after the lapse of some time, from five minutes to an hour—an 
average of about twenty minutes—the patient, either without any 
warning at all, or feeling some irritation at the back of the throat, is 
seized with a paroxysm of cough which nearly chokes him; he feels as 
if he is unable to expel a piece of tenacious mucus which sticks in his 
throat. Finally he vomits out, in part or completely, the gastric con- 
tents which are in a variable state of digestion, according to the time 
they remained in the stomach. There is no sensation of nausea before 
the paroxysm, but the vomiting comes on suddenly during the coughing 
spell; a fact which differentiates this form of vomiting from other forms. 
When occurring for the first time the patient is alarmed, or may be 
inclined to attribute it to some dietetic indiscretion, but if it occurs 
repeatedly he is compelled to seek another cause. As soon as the vomit- 
ing ceases the patient usually feels greatly relieved, the sensation of 
gastric distention and the dyspnea disappear, and at times he may 
express a desire to eat again. After a time the patient learns prudence 
from experience—he knows that a heavy meal may bring about a fit 
of cough followed by vomiting. 

During the course of phthisis there occur also other varieties of 
vomiting which cannot be classified under the heading of emetic cough. 
Patients who have been sufferers from chronic gastritis, dilatation of 
the stomach, and chronic alcoholism, often vomit; at times vomiting 
is provoked by cough. In the advanced stages of the disease vomiting, 
preceded by cough or not, may occur and in some patients it may be so 
pronounced as to preclude feeding. But these forms of the vomiting 
are not the true emetic cough. These patients usually suffer from 
symptoms of indigestion—nausea, furred tongue, foul breath, consti- 
pation, diarrhea, headache, etc. Examination usually reveals a dilated 
stomach, amyloid, or fatty degeneration of the liver, symptoms of 
tuberculous peritonitis, ete. Moreover, while the vomiting may occur 
after coughing, yet it is not invariably preceded by paroxysmal cough, 
occurs irregularly, not always after the ingestion of food, and there is 
no relief immediately after the vomiting. In alcoholics the vomiting is 
more apt to occur in the morning, and this is also the rule with those in 
whom the cough is due to chronic pharyngitis. In both these condi- 
tions, nausea, retching, etc., are common, while in the true emetic 
cough they are absent. The emetic cough often occurs in the early stages 
of phthisis, in patients in whom the gastric functions are in good condition, 
is always preceded by spells of cough, always occurs at a certain time 
after the ingestion of food, 1s not preceded nor followed by sensations of 


COUGH 199 


nausea, giddiness, faintness, and retching. The reverse, vomiting and 
then coughing, vs never observed. 

This form of vomiting, or the emetic cough, is observed in practice 
in but a few diseases, namely, phthisis, whooping-cough, and in certain 
forms of pharyngitis, especially in alcoholics. Recently the writer has 
observed it in many cases of post-influenzal bronchitis and bronchiec- 
tasis. The fact that the thoracic glands are found enlarged in many 
of these cases explains its origin. When whooping-cough is excluded 
in a patient with an emetic cough, the pharynx is found to be in good 
condition, and post-influenzal bronchitis is not suspected, phthisis is 
at once to. be thought of. If it persists, a diagnosis of tuberculosis may 
be made even in the absence of definite physical signs of the disease. 

Some authors have been inclined to look at the emetic cough as a 
mechanical accident, comparable with that observed in whooping- 
cough. But it appears that this does not entirely explain this phe- 
nomenon. If the compression of the abdominal muscles and stomach 
were the sole cause, we should expect vomiting to occur during vio- 
lent and prolonged asthmatic paroxysms. But I have never seen a 
patient suffering from asthma vomit after an attack of cough and 
dyspnea, and be relieved immediately after the gastric contents have 
thus been expelled. 

As has been pointed out by Michel Peter, W. Soltau Fenwick,! 
Paillard, and others, the emetic cough appears to be purely a reflex 
phenomenon, due to irritation by the ingested food of the gastric ends 
of the vagus, and an abnormal excitability of the respiratory center. 
Hence, the slightest irritation of the gastric mucous membrane by 
particles of food is sufficient to produce a violent attack of reflex cough 
which can bring about vomiting in a mechanical manner. 

Cough during the Advanced Stages of Phthisis.— With the advance 
of the disease the cough becomes more and more abundant, more 
productive, but easier, and less exhausting. After the formation of 
cavities, there is usually observed a diminution in the frequency of the 
cough, sleep is hardly disturbed during the night when the reflexes are 
in abeyance, and the secretions accumulate in the cavity. But in the 
morning, when compelled to empty the cavities of the secretions, there 
are fits of coughing lasting several minutes, perhaps an hour, and the 
patient feels relieved. 

These patients, like those suffering from bronchiectasis, suffer from 
cough periodically when the excavations have been filled and need 
emptying. It may be influenced by posture—as soon as they change 
their position, the secretions overflow the bronchial tubes and must 
be brought out by cough, which does not cease until all has been dis- 
charged. Then there is relief for a variable time until the cavity is 
again filled. The patients usually learn from experience on which side 
to sleep if they want to have peace. It is not always on the healthy 


1The Dyspepsia of Phthisis, London, 1894, p. 118. 


200 COUGH AND EXPECTORATION 


side on which they can lie with more or less comfort, because, like in 
bronchiectasis, it depends on the direction of the bronchus, or sinus, 
which empties the cavity. Patients with pleural effusions also cough 
when changing their positions, but in their case the cough is usually 
dry, and is not instrumental in bringing up abundant sputum. [or 
obvious reasons, patients cough more when lying down than when in 
the upright position. But in others sitting up in, or getting out of bed 
excites a paroxysm of cough and expectoration. 

In some cases the cough at this stage is very severe and almost 
incessant, painful, and preventing rest day and night; actually exhaust- 
ing. It is noteworthy that the severity of the cough does not alto- 
gether depend on the extent of the lesion in the lung, nor on the size 
and number of the cavities. Some will cough very little, although the 
lungs are extensively involved, while others, w ith limited infiltrations 
or excavations, cough severely. 

The cough of tuberculous patients is often greatly influenced by 

various factors, of which the age and the emotional state are most 
important. Young adults cough, as arule, more than old consumptives. 
In fact, a large proportion of old people suffering from phthisis hardly 
cough; they bring up large quantities of sputum without any effort. 
They are the patients who supply the material for those who describe 

cases which have been sick with tuberculosis for many years and never 
coughed. The psychic state of the patient also has a great influence. 
The nervous, irritable, and hysterical, cough more than the indolent 
and phlegmatic. The former class is also more apt to suffer from the 
emetic form of cough. 

Diagnostic and Prognostic Significance.— On the whole, cough serves 
a very good purpose by drawing the attention of many patients to 
the condition of their lungs. A person who never coughed, but “caught 
cold” for the first time after his eighteenth year, and as a result keeps on 
coughing for more than a month, rs to be strongly suspected of being 
tuberculous, even if there are no definite physical signs of a pulmonary 
lesion. The suspicion is fortified by a history of the absence of acute 
coryza during the first few days of illness, because simple bronchitis 
and “grippe”’ are almost always preceded or accompanied by rhino- 
pharyngeal catarrh. 

From the prognostic viewpoint cough is important because we 
meet cases with small pulmonary foci without much fever, anorexia, 
emaciation, etc., who would undoubtedly do well, but for a cough 
which is difficult to control. If violent, paroxysmal, and continuing 
for some time, the cough may be instrumental in extending the lesion, 
exhausting the patient, and thus aggravating the outlook. It also 
irritates the larynx, trachea, bronchi, and pulmonary parenchyma, 
and predisposes these organs to infection by metastasis of the bacilli. 
Violent fits of cough may also be responsible for spontaneous pneumo- 
thorax in cases inwhich the lesion is located superficially or subpleurally. 


EX PECTORATION 201 


Kuthy and Wolff-Kisner! say that the most unfavorable prognosis is to 
be given in cases in which the patient coughs during both day and night; 
relativ ely more favorable is the outlook when he Couche during the day 
exclusiv ely; ; more favorable when he coughs only mornings and even- 
ings; and most favorable when he coughs exclusively in the morning. 

W ithin certain limits cough also gives other prognostic hints. With 
each improvement in the local or “general condition, the cough also 
improves or disappears, and with every recrudescence of cough we 
may find an extension of the process in the lungs, or some complication 
in the bronchi or rhinopharynx. Occasionally we may note that the 
sudden disappearance of cough is a signal of some grave complication 
of phthisis, especially meningitis or peritonitis. The same is at times 
seen in cases of severe ulcerations of the larynx, causing dysphagia, 
etc. The cough may be ameliorated, but the lesion in the lungs con- 
tinues or eee and, combined with the exhaustion due to far of 
nourishment, the end is not very far. 

Hoarseness.— Changes in the timber of the voice may appear quite 
early in the disease without any tuberculous involvement of the larynx. 
The least provocation, such as changes in the weather, or prolonged 
speaking, may produce dysphonia, or a muffled voice, without any 
pain which, with the dyspnea preventing speaking continuously long 
sentences, may be quite troublesome. 

In many cases the hoarseness is due to simple catarrh caused by 
local irritation of the larynx by the secretions while they are being 
eliminated from the lungs. In others, pressure of a tuberculous gland, 
lying between the trachea and the esophagus, on the recurrent laryn- 
geal nerve causing adductor paralysis, is the cause. Reflex irritation 
of the superior laryngeal nerve may also be the cause of hoarseness. 
Often the hoarseness is due to tenacious secretions sticking to the vocal 
cords, and after coughing strongly they are dislodged a the voice 
is again normal. Congestion of the larynx caused by violent fits of 
coughing may be the reason for hoarseness. 

It is thus evident that not all cases of hoarseness, or even dysphagia, 
are due to tuberculous ulcerations of the larynx. In fact, no diagnosis 
of the latter condition should be made without a careful and pains- 
taking inspection of the larynx with a mirror by one who is competent 
and experienced. 


EXPECTORATION. 


Careful inquiry reveals in most cases that the cough preceded expec- 
toration by several weeks or even months, and we must not unequivo- 
cally conclude that because the cough is unproductive we are not deal- 
ing with phthisis. Children before the sixth year never bring up any 
sputum at all, because they unconsciously swallow it, and most women 
do the same. I have met with cases in which urging women to expec- 


1 Die Prognosenstellung bei der Lungentuberkulose, Berlin, 1914, p. 219. 


202 COUGH AND EXPECTORATION 


torate was of no avail. Many men are not much better in this regard 
and, for reasons of false delicacy, they swallow the sputum, especially 
during the early stages of the disease. In the advanced stage we may 
meet with the same condition when the emaciated patient is exhausted 
and hardly has any strength to rise, or turn around in bed and expec- 
torate into the sputum cup. 

With the advance of the disease the quantity of sputum eliminated 
increases, but I have met with cases showing extensive infiltrations of 
more than one lobe, without any substantial expectoration, and in 
some of these I have been convinced that they had not swallowed the 
sputum. It was merely an indication that the tubercles had not 
broken through a bronchus, or that the cavities were “dry.” 

Macroscopic Appearance of the Sputum.—There is nothing typical 
about the naked-eye appearance of the matter expectorated in early 
phthisis, although ancient clinicians gave detailed descriptions of 
typical tuberculous sputum. Perhaps the fact that they knew very 
little about early phthisis will account for their confidence in the gross 
appearance of the sputum in this disease. 

In the early stage we find that the sputum is scanty; at times it 
is altogether absent. Kuthy found that in 49 per cent of cases in the 
first stage, 15.4 per cent of the second stage, and 12 per cent of the 
third stage, sputum was altogether absent. What is usually brought 
up in the early stage is viscid mucus, occasionally with some dark 
specks; it is often frothy and floats on water, hardly differing from the 
expectoration in bronchitis. 

With the advance of the disease the sputum becomes thicker, 
although it remains glassy or transparent for some time, but yellow 
streaks are to be seen, indicating that it is assuming a purulent char- 
acter. Later its appearance and consistency change: It becomes 
mucopurulent, and finally purulent, indicating that softening of lung 
tissue has taken place and the necrotic parts are being eliminated. 
The purulent character of the expectoration is judged by the yellow, 
yellowish-green, or green color it assumes. Pure purulent sputum, 
without froth, is mostly seen in cases in which an abscess, an empyema, 
or pyopneumothorax has broken through a bronchus. 

In the far-advanced stage of the disease the sputum is usually dark 
gray, or greenish in color, made up of roundish balls which float around 
like islands in the fluid mucus or saliva or, when thicker in consistency, 
sink down to the bottom of the receptacle, where it settles in disk or 
coin-shaped masses which keep apart and do not coalesce. This is 
the nummular sputum of old physicians which had erroneously been 
considered pathognomonic of phthisical excavations. At times whitish, . 
cheesy masses, derived from broken-down tubercles, are seen scattered 
within this sputum. 

This sputum is usually odorless, but at times it acquires a very 
disagreeable, sweetish, but nauseating odor, especially when retained 
within the chest by narcotic drugs, or weakness of the patient. Fetid 


EXPECTORATION 203 


and offensive sputum is exceedingly rare in phthisis. Whenever it 
is met with in a case of undoubted phthisis we should look for compli- 
cating pulmonary gangrene, which occurs at times. More commonly 
fetid sputum is indicative of some non-tuberculous pulmonary disease, 
especially abscess and gangrene of the lung, malignant disease of the 
bronchi or lung, ete. 

In tuberculosis the sputum is usually salty in the early stages of the 
disease, but later it often acquires a sweetish, sickening taste. 

Very often this sputum, derived from tuberculous cavities, when 
allowed to stand in a vessel for some hours separates into three layers 

—an upper frothy layer; a middle thin serous layer; and a lower 
layer consisting of thick plugs of pus. This is characteristic of excava- 
tion but is not necessarily of tuberculous origin. Bronchiectasis and 
chronic bronchitis with copious expectoration may also be productive 
of sputum which separates on standing. However, in the former the 
lines of demarcation between the layers are not so distinct, but one 
passes into the other by slow gradations. In rare instances calcareous 
masses, “stones,” may be found in sputum derived from tuberculous 
cavities. 

There are cases of advanced chronic phthisis with scanty, or even 
without any expectoration, especially those of the type of fibroid 
phthisis, or with emphysema, although they have periods in which 
the expectoration is quite profuse. The expectoration decreases in 
quantity when the cavities “dry up” during the process of healing, and 
in other types of cases when the concomitant bronchitis disappears. 
With but few exceptions, scanty expectoration speaks for a favorable 
outlook, provided the temperature is normal and the cough is also 
absent or mild. On the other hand, copious expectoration per se is 
not always an unfavorable sign. It is an indication of excavation, 
bronchitis, or bronchiectasis which are not infrequent in phthisis. In 
the latter cases the sputum may show a tendency to collect and be 
expelled at intervals in very large quantities—mouthfuls—without any 
effort, and may also be influenced by posture. 

During hemoptysis the material expectorated is sanguineous in 
various degrees, corresponding to the severity of the bleeding, and for 
a few days after the cessation of the active hemorrhage the sputum 
contains dark clots derived from the blood that has coagulated in the 
excavations or the bronchi and is being slowly eliminated. The sputum 
may have a reddish or chocolate tinge without distinct hemorrhage, 
and even viscid, rusty sputum characteristic of pneumonia is at times 
encountered in phthisis. Inasmuch as this is, as a rule, seen during 
an acute exacerbation of fever, etc., I am inclined to account for it, 
in many cases, by intercurrent pneumonia. In the terminal stage of 
advanced cases I have often seen thin, watery sputum, dark brown in 
color, with numerous air bubbles—prune-juice sputum—which is an 
indication of pulmonary edema. Green sputum is at times met with, 
and is usually ascribed to the implantation of the Bacillus pyocyaneus 


204 COUGH AND EXPECTORATION 


In eases in which a pyopneumothorax communicates with a bronchus, 
as well as when an empyema breaks through a bronchus, the sputum 
may be distinctly purulent, and I have seen cases in which the empyema 
was thus cured, though the tuberculous process went on its course. 


EXAMINATION OF THE SPUTUM. 


Collection of Specimen.—In cases of suspected phthisis the sputum 
gives important information which is often of more value than all 
other diagnostic methods for this disease taken together. This is 
especially true of the microscopic examination. 

It is important, especially in cases with scanty expectoration, that 
the specimen of sputum for examination should be properly collected. 
The patient must be warned that what we want is material that has 
been coughed up from beneath the glottis, and not what has been 
hawked out from the rhinopharynx, or saliva. A clean, wide-mouthed 
bottle is the best receptacle, and it should be tightly corked. The one 
used by the Health Department in New York City is excellent. In 
cases with scanty expectoration, a twenty-four-hour specimen is 
desirable, but with others the quantity coughed up during the morning 
on rising is sufficient. Fresh sputum is best, but putrefaction does 
not interfere with the appearance of the bacilli under the microscope. 

It must be emphasized that really active cases of tuberculosis with 
persistently negative sputum are rare. Most of these cases, if examined 
repeatedly, w il show the presence of tubercle bacilli in the sputum. 
In my wards at the Montefiore Hospital we often find that these 
“closed” cases show the presence of bacilli after several examinations 
of the sputum. In some it takes as many as twenty microscopic 
examinations to find one positive. But it is doubtful whether a patient 
who shows persistently negative sputum is in fact sick with tubercu- 
losis requiring treatment, and I have been under the impression, based 
on good evidence, that the sanatoriums which have as many as over 
50 per cent of “sputum negative” cases have an enormous proportion 
of non-tuberculous cases within their walls. I doubt whether more than 
10 per cent of these “sputum negative” cases are tuberculous in the 
clinical sense. 

On the other hand, it is wrong to consider a case as not contagious 
because the sputum is negative. We are of late beginning to realize 
that the sputum is not the only vehicle in which tuberculosis is trans- 
mitted from the sick to the well. This point has been discussed in 
detail elsewhere in this book. 

Microscopic Examination.—In the very early stages of active phthisis 
tubercle bacilli are more often absent than present in the sputum, and 
it is only after softening of tubercles has taken place and the diseased 
focus opens into a bronchiole that they can be found. In general, it 
may be stated that severe cases show large numbers of bacilli, but there 
are many exceptions. In fact, in acute pneumonic phthisis bacilli are, 


EXAMINATION OF THE SPUTUM 205 


as a rule, lacking. The absence of bacilli is therefore not conclusive 
proof of the non-tuberculous character of a case, because we meet with 
undoubted cases of active and progressive tuberculosis, proved by 
subsequent autopsy findings, in which no bacilli were discovered 
throughout the course of the disease. In general, it may, however, be 
stated that these “closed” cases of tuberculosis run a more favorable 
course. On the other hand, in acute miliary tuberculosis, tubercle 
bacilli are discovered in the sputum in exceedingly rare instances. 

In early phthisis in which it is difficult to obtain sufficient sputum 
for examination, the administration of iodides, 5 grains three times 
a day for a couple of days, may increase the amount of expectoration. 
We may, in some cases, also administer an opiate in the evening with a 
view of retaining the sputum during the night, so that it may be 
brought up in the morning on rising. In children, swabbing the 
throat with some gauze, as suggested by Holt, may yield a specimen 
for examination, though in my hands it has invariably failed. 

Technic.—The examination is best and most rapidly accomplished 
by the Ziehl-Neelsen, the Gabbet, or the Hermann methods, which 
have survived numerous modifications introduced during recent years. 
Details have been given on page 18. 

With a platinum-wire loop a cheesy or mucopurulent particle is 
picked out and spread over a perfectly clean cover-glass in a thin, 
uniform layer. It is even better that a small amount of sputum 
should be spread between two cover-glasses which are drawn apart. 
The cover-glass is dried in the air, or over a Bunsen burner at some 
distance from the flame. When dry, it is “fixed” by passing it three 
or four times through the flame. Some carbol-fuchsin solution is put 
on the specimen which is picked up with a Cornet forceps and held over 
the flame for about three minutes or more until it steams. It is then 
decolorized in a 10 per cent solution of nitric acid, or a 10 per cent 
solution of sulphuric acid and washed in 60 per cent alcohol, until it is 
faintly pink or completely colorless, when it is counterstained with an 
alcoholic solution of methylene blue, washed in water, and dried 
between filter paper. 

With Gabbet’s method the staining with carbol-fuchsin is the same 
as above, but the decolorization and counterstaining are done together 
by placing the specimen in Gabbet’s solution (see p. 19). 

The Hermann stain is also easy; it consists in: (a) Crystal violet, 
3 per cent in alcohol; (6) ammonium carbonate, 1 per cent solution in 
water. Mix one part of solution a with three parts of solution b just 
before using. Steam as above, decolorize with 10 per cent nitric acid, 
wash in alcohol, and counterstain with Bismarck brown. At times 
this method will reveal bacilli when the above have failed. 

These methods will disclose the bacilli in the vast majority of cases, 
but they fail at times because of the small amount of sputum avail- 
able, or the small number of bacilli present in the specimen, or the 
selection of a particle of sputum with the platinum loop which does 


206 COUGH AND EXPECTORATION 


not contain any bacilli. To obviate these sources of error there have 
been devised new methods which liquefy the sputum, digest all the 
cells and bacteria which may be present, excepting the tubercle bacilli, 
which can be centrifuged and be examined microscopically, and may 
even be used for cultural purposes, or for injections into animals. The 
antiformin method is at present the best and simplest available for 
the purpose. 

The Antiformin Method.—This method, devised by Uhlenhuth and 
Xylander, and modified by others, consists in mixing the sputum 
with antiformin—a strongly alkaline mixture of sodium hypochlorite, 
equivalent to 5.68 gms. available chlorine; sodium hydroxide, 7.8 
gms., and sodium carbonate, 0.32 gm.—used by brewers in the disin- 
fection of their fermentation vats and tubes. When properly diluted 
and mixed with sputum, there is a strong liberation of gas, the insol- 
uble organic matters, as well as bacteria, are destroyed, excepting hair, 
fat, wax and cellulose, and acid-fast bacilli, the vitality and staining 
reactions of which remain unchanged. The resulting yellowish solu- 
tion is a homogeneous mixture with a flocculent sediment. Because 
it has a fatty capsule the tubercle bacillus remains intact while all 
other microdrganisms are rapidly destroyed. 

Of the various modifications of Uhlenhuth’s original method, the 
one devised by Boardman! is the most serviceable. It consists in: 

1. Place the entire twenty-four-hour sputum in a conical settling 
glass; if the amount is excessive it is perhaps better to use only 15 to 
20 ce. 

2. If the specimen is thick, add an equal volume of distilled water. 
Less tenacious specimens do not require so much dilution. 

3. Add an amount of antiformin equal to one-fourth the volume of 
the diluted sputum; in other words, sufficient to make a 20 per cent 
solution. 

4. Stir thoroughly, thereby breaking up the masses of mucus and 
greatly hastening complete solution. 

5. Allow to stand till solution appears homogeneous. It should now 
be watery in consistency and pale yellow in color; if necessary, more 
water or more antiformin should be added and digestion allowed to 
continue. ‘This will usually require from a few minutes to an hour, 
but may be allowed to continue for days with no resulting harm to 
the tubercle bacilli. 

6. Add an equal volume of 95 per cent alcohol. By this procedure 
the specific gravity is reduced from about 1.030 to below 1; thereby 
not only hastening sedimentation, but making it more complete. 

7. After stirring, allow to stand till sedimentation is complete. This 
will occur in from two to four hours, but a period of twelve to twenty- 
four hours is recommended. During this sedimentation it may be 
necessary to gently turn the vessel to dislodge little particles of sedi- 
ment which may be adhering to the sides of the vessel. 


1 Johns Hopkins Hosp. Bull., 1911, 22, 269, 


EXAMINATION OF THE SPUTUM 207 


8. Pour off the clear supernatant fluid. 

9. Make a smear from the sediment on a glass slide, using some of 
the original sputum to aid in fixing the smear. This is best done by 
making a smear from the sputum before antiformin is added and 
afterward spreading the sediment from the sputum-antiformin mixture 
on the same slide. Stain in the usual way. 

There are many modifications of this method which do not require 
twenty-four hours for execution. Loeffler’s modification, which takes 
but ten minutes, is the best: 

A certain quantity of sputum (10 to 20 ce) is mixed with an equal 
quantity of 50 per cent aqueous solution of antiformin and _ boiled 
over the flame. Rapid liquefaction is observed. To each 10 cc of 
the mixture, 1.5 ce of a 10 per cent alcoholic solution of chloroform 
is added. tier stirring for some time the solution is centrifuged for 
about fifteen minutes. The disk which forms on the surface of the 
chloroform contains the tubercle bacilli, and is to be pipetted, fixed 
with egg albumen, and stained in the usual way. 

Theophile Raphael’s! modification of Greenfield and Anderson’s? 
method is even more reliable and time-saving. The procedure is as 
follows: 

Five cc of sputum, to which have been added two volumes of 1 per 
cent solution of sodium carbonate in | per cent phenol, are shaken for 
ten minutes and then autoclaved for twenty minutes at fifteen-pounds 
pressure. Following this, the material is centrifuged for ten minutes, 
the supernatant fluid decanted, and sthears are made and stained from 
the sediment. The following reagent is employed: Equal parts of 
15 per cent sodium hydroxide and Labarraque’s solution. Five parts 
of sputum with one part of reagent are shaken for fifteen minutes, 
incubated for one hour, and then centrifuged for fifteen minutes. The 
supernatant fluid is decanted and the sediment washed by centrifuging 
for fifteen minutes with distilled water. Smears are made and stained 
from the sediment. 

The great importance of the antiformin method lies in the fact that 
it exerts a destructive action on all cells and microérganisms excepting 
the acid-fast rods which may then be found microscopically. - But 
soon after its introduction it was found that acid-fast rods which are 
not pathogenic, and which are often found while looking for tubercle 
bacilli, may escape destruction by the antiformin, thus causing mis- 
takes. Especially was the question whether the smegma bacillus is 
dissolved by this agent important. In a recent investigation of this 
problem by von Spindler-Engelsen,’ she found that the smegma, the 
timothy-hay bacillus, the butter bacillus, etc., are dissolv ed by 15 
per cent of pariternin | in thirty minutes. The human and the bovine 
types of tubercle bacilli were not affected with a 50 per cent antifor- 


1 Jour. Am. Med. Assn., 1920, 75, 245. 
2 Lancet, 1919, 2, 423. 
3 Centralbl. f. Bakteriol., 1915, 76, 356, 


208 COUGH AND EXPECTORATION 


min solution for four days. Under the circumstances it appears that 
the pathogenic bacteria may be discovered with the aid of this method. 
It is, however, important that a fresh solution of antiformin should 
always be used, because a weak and old solution may leave the non- 
pathogenic bacteria and thus lead to error. 

Much’s Granules.—As has already been stated, there are cases of 
pulmonary tuberculosis in which no acid-fast bacilli can be discovered 
in the sputum by any method, and Much has shown that they are 
due to a certain kind of bacilli which have lost their acid-fast property, 
but are Gram-positive and they retain their virulence. According to 
some authors these Much granules are almost always found in cases 
of fibroid phthisis, chronic bronchitis, emphysema, bronchiectasis, etc., 
in which acid-fast bacilli are very rarely discovered (see p. 19). Much 
found them in cases of cold abscess. 

As to the reasons why the bacilli lose their acid-fast properties, there 
is no agreement. It also appears that the proportion of cases in which 
they are found varies with different observers, some having detected 
them in as many as one out of eight sputa, while others in less than 
2 per cent. Much gives several methods for staining these granules. 
The following is the most suitable: 

A very thin smear is made of the sputum and allowed to remain for 
twenty-four to forty-eight hours in a methyl-violet solution (methyl- 
violet, 10 ce of a saturated solution, in 100 ec of a 2 per cent watery 
solution of carbolic acid) at 37° C. temperature; or it may be stained 
by boiling for a few minutes over the flame. Wash and stain for one 
to five minutes with Gram’s iodine and put for one minute in a 5 per 
cent nitric acid solution, then in a 3 per cent hydrochloric acid solu- 
tion for ten seconds, and finally complete the decolorization by placing 
it for a few seconds in acetone-alcohol (equal parts of acetone and 
alcohol). Wash and dry. 

Prognostic Value of Microscopic Findings.—The interest displayed by 
many patients, as well as by physicians, in the number of bacilli 
found in a specimen of sputum examined with a view to drawing prog- 
nostic conclusions is unjustified. There are cases which show but few 
bacilli in each specimen, yet they run a very acute and progressive 
course, while others with numerous bacilli pursue a slow, chronic 
course, terminating in recovery. Especially is this seen in senile 
phthisis, in which the number of bacilli expectorated is enormous and 
we may, in fact, speak of pure cultures; yet these “bacilli carriers” 
live on for years with comparative comfort. Of course, in such cases 
we may deal with a small ulcerating cavity in the lung which offers 
good opportunities for the growth of bacilli, but the fibrous capsule 
prevents the extension of the lesion. 

The number of bacilli in the sputum fluctuates from day to day, 
evidently depending to some extent on the bit of sputum we happen 
to pick up with the loop. On the other hand, the complete absence 
of bacilli from the sputum for several weeks, coupled with improve- 


EXAMINATION OF THE SPUTUM 209 


ment in the general condition of the patient, is undoubtedly a favor- 
able sign. But many chronic cases, especially fibroid phthisis, are 
always “closed”’—bacilli are scanty or absent. With modern methods 
of antiformin examination of sputum the number of active, but ‘‘closed”’ 
cases has been reduced very much. In addition to the tubercle bacilli, 
various other microédrganisms are frequently found in the sputum of 
tuberculous patients. They are usually saprophytes, and have no 
influence on the symptomatology and course of the disease. In contra- 
distinction to this “passive mixed infection,” we meet with “active 
mixed infection,” in which the organisms, pneumococci, Pfeiffer’s 
bacilli, streptococci, staphylococci, etc., are responsible for compli- 
cating processes. These are discussed elsewhere in this book. 

Inoculation.—In cases in which it is very important to decide the 
problem whether we are dealing with active tuberculosis, and the 
bacilli are too few in number to be demonstrated by the ordinary 
microscopic methods, or after concentration of the sputum, inocula- 
tion of a susceptible animal often leads to a decision. In this regard, 
it must always be remembered that the susceptibility of ordinary 
laboratory animals to the tubercle bacilli varies greatly. The white 
mouse and the rat are relatively insusceptible. So is the rabbit to the 
human type of the bacillus, but it is very susceptible indeed to the 
bovine type. Hence, inoculation of the rabbit is a substantial aid in 
the differentiation of the human from the bovine species. The guinea- 
pig is exceedingly susceptible to both mammalian types of the tubercle 
bacillus, and is the animal ordinarily used for inoculation with material 
suspected of harboring tubercle bacilli. 

If the material to be inoculated into the guinea-pig is very badly 
contaminated with other bacteria, it is best to subject it to the action 
of antiformin; but this should not be carried too far, lest the virulence 
of the tubercle bacilli themselves be seriously impaired. The material 
is suspended in sterile salt solution (though sometimes solid blocks of 
tissue or sputum are placed under the skin and the wound protected 
with cotton and collodion) and injected intraperitoneally, or subcu- 
taneously, or better, perhaps, in both sites. The intraperitoneal injec- 
tion gives quicker results, but there is greater possibility of losing 
the animal through a non-tuberculous infection before tuberculosis 
can develop. An autopsy performed four to six weeks after intra- 
peritoneal injection, if tubercle bacilli were present in the suspected 
sputum, will show widespread tuberculous lesions of the peritoneum, 
the omentum, the retroperitoneal lymph glands, the spleen, the liver, 
and sometimes the lungs. Examination after subcutaneous injection 
of the suspected material, when positive, shows a caseating lesion at the 
site of the inoculation, also similar lesions in the regional lymph glands, 
liver and spleen. In addition to caseous lesions of the viscera, large 
areas of necrosis are often seen, One should never be content with the 
gross appearance of the lesions, but should always stain sections for 
Koch bacilli, which are usually present in large numbers. By removal 

14 


210 COUGH AND EXPECTORATION 


of enlarged glands with the animal etherized, the bacilli can often be 
demonstrated in section after ten to fourteen days. 

There are, however, in rare instances, cases in which it is of great 
importance to ascertain the presence or absence of tubercle bacilli in 
the sputum sooner than in six or eight weeks. Some have suggested 
that after the suspected material has been injected into the abdominal 
wall or the peritoneum, the animal should be tested at frequent inter- 
vals with tuberculin. A positive reaction clears up the case (R6mer 
and Joseph'). F. Gratz? has used the intracutaneous method. He 
inoculated 1000 guinea-pigs and then applied the intracutaneous tuber- 
culin test and found that in ten or twelve days after the inoculation 
of the infectious material a positive diagnosis may be made. Martin 
Jacoby and N. Meyer*® suggest that the sputum be injected into a 
guinea-pig and about fourteen days later 0.5 ce of tuberculin should 
be injected subcutaneously. If the sputum contains tubercle bacilli 
and infects the animal, it will die from anaphylactic shock within a 
few hours. 

But these methods are not infallible. Seltert shows that a posi- 
tive reaction in an inoculated guinea-pig indicates that infection has 
taken place, while a negative result does not prove the contrary. 
The autopsy alone is conclusive. Many guinea-pigs inoculated by 
Selter with small doses of virulent bacilli were found to give negative 
results to the intracutaneous test, while the autopsy revealed marked 
tuberculous changes in various organs. 

It must also be mentioned in this connection that guinea-pigs are 
often tuberculous spontaneously. Many authors have reported that 
they found tuberculous lesions in these animals. Sir Almroth Wright, 
Frank J. Clemenger and F. C. Martley® point out that great difficulties 
are encountered in obtaining guinea-pigs free from pseudotuberculosis; 
a large proportion of the animals were found affected with various forms 
of this disease. In a lot purchased from a guinea-pig fancier who bred 
his animals exclusively for purposes of exhibition, and which were 
young and, from all outward appearances, perfectly healthy, a point 
was made to autopsy with great care each of the animals of this lot 
that had been killed for the purposes of securing fresh serum for com- 
plement, and pseudotuberculous lesions were found in every one of 
them. “The amazing point about these infections with pseudotuber- 
culosis is the large amount of vital organs which can be involved in 
the local process and yet permit the animals to live in apparent health.” 
The possibility of error while utilizing guinea-pigs for diagnostic 
experiments is manifest. 

Elastic Fibers.— Before the discovery of the tubercle bacillus great . 
stress was laid on the presence or absence of elastic tissue in the 


1 Beitr. z. Klin. d. Tuberk., 1909, 14, 1. 2 Ibid., 1916,-36, 99. 
3 Tbid., 1911, 20, 263. 

4 Deutsch. med. Wehnschr., 1916, 42, 77, 283. 

5 Senate Document No. 453, Washington, 1916. 


EXAMINATION OF THE SPUTUM 211 


sputum in the diagnosis of tuberculosis, but of late this is only rarely 
looked for. It is, however, a simple thing to find elastic tissue when 
present in the expectoration, and it is of immense diagnostic signifi- 
cance because it can be found in over 90 per cent of tuberculous sputa. 
The presence of elastic fibers in the sputum is an indication of 
destruction of lung tissue and it may be found in the very early stages 
of the disease, because chronic tuberculosis is a destructive process, 
and small excavations may be found quite early, and the elastic fibers 
are not destroyed during the caseous degeneration which liquefies the 
pulmonary tissue. They are also found in gangrene, abscess, syphilis, 
and infarction of the lung, so that when the latter can be excluded, they 
may greatly assist in the diagnosis of doubtful cases of tuberculosis. 





Fic. 33.—Elastic fibers in the sputum. (v. Jaksch.) 


Technic.—A small amount of the thick, purulent portion of the 
sputum is pressed into a thin layer between two pieces of plain window- 
glass, 15x 15 cm. and 10x10 cm. The particles of elastic tissue 
appear on a black background as grayish-yellow spots, and can be 
examined in situ under a low power. Or, the upper piece of glass is 
slid off until the piece of tissue is uncovered, when it is picked out and 
examined on a slide, first with a low and then with a high power 
(Simon). 

A simpler method is the following: A bit of purulent sputum and 
a drop of 10 per cent solution of sodium or potassium hydroxide are 
placed between a cover-glass and a slide and examined with a mod- 
erate power under the microscope. ‘The elastic tissue is to be looked 
for especially at the border of the preparation. 

If the fibers are scanty they may not be found in this way, and the 
following method may reveal them: The sputum is boiled with a 
10 per cent solution of KOH and well stirred during the boiling. 
When a homogeneous mixture is obtained, it is diluted with four times 
as much water, well shaken, and allowed to stand in a conical glass, 
or centrifuged. The sediment contains all the elastic tissue, which 
may be found under the microscope. 


212 COUGH AND EXPECTORATION 


The different methods of staining elastic tissue are not necessary 
because either of the above methods is sufficient for diagnostic purposes. 

Cytology of Sputum.— Various attempts have been made to assign 
diagnostic and prognostic significance to the cytology of tuberculous 
sputum, especially to the leukocytes and lymphocytes, but without 
avail. Nothing diagnostically important can be learned from a study 
of the white blood cells in the sputum, so far as we know at present. 

Chemical Examination.—The chemistry of the sputum in pulmo- 
nary tuberculosis has not yielded any important diagnostic or prog- 
nostic data, excepting the albumin reaction, which is of great value 
in doubtful cases and is often of assistance when the microscope fails 
to reveal tubercle bacilli. Sputum with a positive albumin reaction 
can be found in tuberculosis and also in cases of pulmonary emphysema 
with cardiac dilatation, pneumonia, pleurisy with effusion, etc., but 
never in uncomplicated bronchitis. 

A positive albumin reaction is not always decisive of tuberculosis, 
but the negative outcome, when persistent during several examina- 
tions, undoubtedly excludes phthisis.'. In some cases of advanced 
tuberculosis, especially fibroid phthisis, the albumin reaction is nega- 
tive, but in such cases the diagnosis is only rarely a problem. It also 
appears that with the improvement in the condition of the average 
patient, the amount of albumin in the sputum decreases and finally 
it disappears. It is thus of prognostic value. 

Technic.—The albumin test is made as follows: A 3 per cent solu- 
tion of acetic acid is added to the sputum, which is then thoroughly 
shaken. During ten or fifteen minutes the bottle is allowed to stand, 
and repeatedly shaken during this time. It will be observed that the 
mucus is coagulated by the acetic acid, and when it is then filtered 
through paper into a test-tube, the filtrate appears as a clear fluid. 
Occasionally all the mucus is not coagulated with the first attempt, 
and this is easily ascertained by adding a drop of acetic acid to the 
filtrate, which in such cases again shows flocculi collecting as a pre- 
cipitate. The process is then repeated until a clear filtrate is obtained. 
The clear fluid is next boiled over a Bunsen burner or an alcohol lamp, 
and while boiling some crystals of common salt, or a concentrated 
solution of sodium chloride are added. 

If albumin is present, there results a cloudiness, or a curdy precipi- 
tate which, on standing, settles to the bottom of the tube. Roughly 
speaking, the amount of the precipitate gives an idea of the amount 
of albumin present. The most important precaution to be observed 
is that nothing but a curdy precipitate should be considered as posi- 
tive, because the presence of mucus, which the acetic acid does not. 
always completely dissolve, may also give a cloudy precipitate on 
boiling. But this precipitate is not curdy, nor does it settle on standing. 
Of course, any other test for albumin may be applied to the filtrate, but 
the above gives satisfactory results. 


1 Fishberg: Med. Press and Circular, 1912, 94, 352; Arch. of Diag., 1912, 5, 220. 


C Hea PRE Rex: 
FEVER AND NIGHTSWEATS. 


FEVER. 


FrvER is one of the first symptoms of active phthisis—perhaps the 
first. It does not run a characteristic course in every case like that 
in malaria, pneumonia, or typhoid fever; in fact, its polymorphism is 
noteworthy. Yet it is of immense diagnostic and prognostic value. 
Some authors state that the fever in incipient tuberculosis is invari- 
ably due to some complication. But the febrile reaction after the 
administration of tuberculin, as well as in acute miliary tuberculosis, 
shows clearly that this view is incorrect. All the available evidence 
combines to prove that it is due to absorption of the poisons produced 
by the tubercle bacilli, though it may be modified by mixed infection. 
The fever is engendered mainly by the increased production of heat— 
the result of complex biochemical processes having their origin in the 
struggle of the organism with the bacilli; the body summoning its 
defensive forces against the toxins produced by the metabolic processes 
of the bacilli and decaying tissues which stimulate the heat regulating 
center. In evaluating the significance of fever in tuberculosis, ut must 
be borne in mind that it 1s not the cause of the disease, but a result of its 
activity. 

Fever ws present in nearly all cases of active disease. In the later 
stages, especially in fibroid phthisis, we often meet with afebrile 
periods of shorter or longer duration, but with each exacerbation of the 
disease, with each extension of the process in the lungs, there is always 
a pronounced rise in the temperature which should be studied if the 
evolution of the case is to be followed. ° 

Thermometers.— The reason why there are found so many apyretic 
cases of phthisis 1s mainly faulty technic in taking the temperature, 
especially defective thermometers. 

The clinical thermometer is an instrument of precision, and when 
used for the purpose of ascertaining the temperature in incipient 
phthisis, in which 1° is occasionally of immense importance in diag- 
nosis and prognosis, it must be accurate. It is, however, a well-known 
fact that, despite the certified accuracy of each instrument, simul- 
taneous observations made on a single patient with two instruments 
often disclose a difference in readings of 0.75° to 2.°. The simultaneous 
immersion of two dozen thermometers in a bath of warm water dis- 
closed that the readings varied from 98.2° to 101.6° F.; another 
similar batch of higher-priced thermometers in another bath showed 


214 FEVER AND NIGHTSWEATS 


variations of temperature between 98° and 105.4° F.! “Certified”’ 
thermometers in this country are not much better. Bray? reports 
that out of a series of 83 certified thermometers tested in a water- 
bath, 17 showed a variation of 0.3° to 0.6° F. Comparative rectal 
readings approximated closely the discrepancies shown in the water- 
bath. The presence or absence of fever, when such thermometers are 
used to ascertain it, depends on the instrument which the physician 
happens to possess and not at all on the condition of the patient. 
Under the circumstances, it is clear that when searching for fever in 
tuberculous patients or suspects, the instruments must be reliable and 
of tested accuracy, otherwise grave diagnostic mistakes of omission or 
commission are likely to occur. 

Technic of Taking the Temperature.— After having a good ther- 
mometer, we must exercise great care in the method of taking the tem- 
perature. I have been so often misled by readings taken in the axilla, 
sometimes finding it as much as 3° below that recorded in the rectum, 
that I now completely discard it. And, strange to say, I meet with 
no patients who refuse to take their temperature per rectum. It has 
been found that in some cases the temperature in the axilla is higher 
on the affected side and urged as a good sign of phthisis, but it is so 
rare that it may be disregarded. 

The mouth temperature is also unreliable to a certain extent. Here 
it is influenced by the temperature of the external air which must be 
inhaled now and then, especially by patients suffering from nasal 
obstruction. The part of the instrument outside the lips, and at times 
also the part within the mouth, are chilled by the external air, more 
often in dyspneic patients. The instrument must be left in the mouth 
at least seven minutes, and it often takes at least ten minutes before 
the mercury rises to the highest point, even with the so-called “minute 
thermometers.’’ On the other hand, in patients suffering from stoma- 
titis, the local temperature may be much higher than that of the blood. 
The temperature in the mouth should also not be taken immediately 
after meals, after taking hot or cold drinks, after washing the mouth 
or brushing the teeth, etc. Many patients are unable to keep the 
thermometer properly beneath the tongue, all surrounded by buccal 
mucous membrane, and avoid breathing through the mouth, or talking 
for five to ten minutes. 

It appears that the majority of physicians in sanatoriums are in 
favor of oral readings because they are dealing with patients who 
practically always associate in groups and cannot use the rectal method 
unless they retire to their rooms for the purpose several times a day. 
This drawback does not hold with bed-ridden patients, and also with 
the average clientele in the city. In fact, I found that suspects, who 
keep at their work while under medical observation, prefer the rectal 
method which they take in the lavatory and thus obviate observation 


1 Lancet, October 4, 1913; November 8, 19138, p. 1842. 
2 Am. Jour. Med. Sci., 1915, 149, 838. 


FEVER 215 


by others. In my hospital work also, there is no trouble in taking 
rectal temperature in walking patients. 

That the rectal method is superior and less likely to mislead is now 
acknowledged by all who have given both methods a trial. In the 
rectum or vagina the instrument is on all sides surrounded by mucous 
membrane, holding it in place as long as necessary and giving reliable 
readings. It has been found that the rectal is almost invariably 0.5° 
to 1° F. higher than the mouth temperature (Fig. 34). Some writers 
state that after exercise the local temperature in the rectum rises, 
while it remains normal in the blood, and for this reason they prefer 
mouth readings. But this again may be explained by the greater 
exactitude of the rectal temperature. It is needless to add that the 
instrument is to be left in the rectum sufficiently long to obtain the 
maximum reading. In my instructions to patients and nurses, I tell 
them that I do not know of any one-minute thermometers, and all 
are to be left in situ at least five minutes. 






















































































































































































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Fia. 34.—Comparative oral and rectal readings of temperature. (Bray.) 


Frequency of Taking the Temperature.—'The habit of many physi- 
cians of taking the temperature when the patient visits them and 
recording it as normal, or elevated to a certain degree, is altogether 
wrong. In early, or doubtful, cases taking three readings a day may 
be misleading, at times, because rises in temperature which occur late 
at night, or early in the afternoon, and are short-lived, may thus be 
overlooked and the patient pronounced free from fever. For reasons 
which will soon be evident, we must, in incipient cases, have a record 
of the temperature taken every two hours, and this is best recorded by 
plotting a curve on a chart which shows graphically any hypothermia 
or hyperthermia. 

Intelligent patients may be entrusted with a thermometer, provided 
they are trained in reading it correctly, which can be done in a few 
minutes. I have had patients who kept records of their two-hourly 
temperature for weeks and, for obvious reasons, more conscientiously 


216 FEVER AND NIGHTSWEATS 


than the average nurse. Many have done it without leaving their 
occupations by simply going to the lavatory every two hours for five 
minutes. 

The Normal Temperature.—It may be stated that the normal 
temperature in children is not a constant value. It is subject to such 
oscillations during perfect health, that any average which has been 
fixed by various authors is only arbitrary. The slightest disturbance 
in health is likely to increase the temperature in the child to a greater 
degree than in the adult. Many clinicians consider a temperature 
of 100° to 101° F. normal in a child, unless there are symptoms of 
disease. But with advancing age the temperature becomes more and 
more settled, so that in adults it is subject to lesser oscillations, unless 

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Fie. 35.—Fever in incipient tuberculosis showing marked subnormal temperature 
in the early morning hours. Temperature taken twice daily. 


As an arbitrary guide for the clinician it may be assumed that a tem- 
perature of 98.6° F. when taken by mouth, and 0.5° higher when taken 
by the rectum, is normal. But even this shows striking diurnal varia- 
tions in normal individuals. During the early morning hours, before 
the individual leaves his bed, it is slightly subnormal by 0.5° to 1°; 
but it rises to normal soon after rising, and keeps quite steady during 
Hak ee Bardswell and Chapman! found an average for w aking hours 

°F ., and for sleeping hours 97.2° F., taken by mouth, which i is in 
He wren with the observations of most physicians. 

There are, however, individuals in whom the temperature is lower than 
the above average and in whom a physiological normal temperature should 
be considered febrile. This is occasionally seen in tuberculous patients 
with subnormal temperature; when the thermometer registers 99° F. 
they present symptoms of fever, such as flushing, hot skin, headache, 
CLC: 

Normally the temperature is elevated in persons after exercise, and 
in some even after a hearty meal. In women it may be higher by 1° or 


1 British Med. Jour., 1911, 1, 1106. 


FEVER 217 


2° before, or during menstruation. But the elevation after exercise 
is, in the healthy individual, evanescent; within one-half to one hour 
it sinks again to normal. 

Other influences which should be mentioned are the emotional 
state of the individual. Particularly in women, excitement may raise 
the temperature 1° to 2°. Where there is a question of tuberculosis, 
the excitement attending the taking of the temperature may be effec- 
tive in raising it, as I have seen in several cases, and we must be very 
careful in making a diagnosis of incipient phthisis on the thermometrical 
readings alone in emotional women. Frank B. Wynn,! in a recent 
study of the subject, found that psychic influences very frequently 
raise the temperature of healthy individuals. Observations made on 
two series of persons under circumstances of considerable nervous 
tension, suspense, and anxiety, such as physical examination during 
the selective draft, students and nurses taking State Board examina- 
tions, etc., showed distinct elevation of temperature in a large propor- 
tion of cases, the degree of elevation varying directly with the gravity 
of the situation facing the individuals. In fact similar observations 
have been made on animals. The frightened rabbit, tied to the opera- 
ting board, shows elevation of temperature, as has been found by 
Moore.” 

In some people who work during the night, and sleep during the 
day, the variations in temperature mentioned above are said to be 
reversed. 

In evaluating thermometrical findings in suspected incipient phthisis, 
we are on safe ground when we consider the normal temperature during 
the day in a person who works, or walks around, as 99° F., when 
taken per rectum, and 0.5° to 0.75° lower when taken by mouth. It 
may be 0.5° to 1° lower in the morning before rising, and 0.5° higher 
in the evening after a heavy meal, or after a hard day’s work. Dis- 
tinct variations from these figures demand explanation, and if no 
other cause is found, tuberculosis is to be considered as the possible 
cause. 

Fever in the Incipient Stage.— When taken with due precautions 
it will be found that a subfebrile or febrile temperature is characteristic 
of the evolution of active phthisis even in the incipient stage, and that the 
absence of fever excludes active disease. The afebrile cases of phthisis 
mentioned by physicians are mostly the result of faulty technic in 
taking the temperature. Evanescent rises are overlooked. Moreover, 
in these cases the instability of the temperature could be determined 
by ordering the patient to take some exercise. An elevation of ().5° 
to 1.5° in the afternoon, or after some excitement, or exertion, lasting 
about half an hour may be observed in some persons who have no 
tuberculosis, as was mentioned above; with the phthisical, however, 
it is more lasting. It appears that a large proportion of patients with 


1 Jour. Am. Med. Assn., 1919, 62, 31. 
2 Am. Jour. Physiol., 1918, 46, 244. 


918 FEVER AND NIGHTSWEATS 


early tuberculosis have a subnormal temperature in the early morning 
hours, some recording as low as 96° F., before getting out of bed. 

When interpreting fever in the early stages of phthisis, we should 
follow Daremberg’s! suggestion and consider the difference between 
the highest and lowest temperature. Thus, a patient with a tempera- 
ture of 99.8° F. at 5 p. M. has not only 1° above normal when his morn- 
ing temperature is 96.5° F., but 3.3° above normal, and should be con- 
sidered febrile, and when persisting for some time, it is undoubtedly of 
tuberculous origin, unless some other cause is found. 

Symptoms of Fever.—These afternoon rises can also be distin- 
guished from other rises, and from physiological elevations, by the 
concomitant symptoms which are met with in most cases of incipient 
phthisis. In the latter there is an acceleration of the pulse-rate far 
out of proportion to the slight elevation of temperature. Many also 
have mild chilly sensations, or even a distinct chill, about an hour 
before the rise in temperature, when the face is pale, and the extremities 
feel cold. Later the face becomes flushed, the eyes brighten with 
characteristic brilliancy, which can often be recognized by the experi- 
enced observer, and the patient feels warm or hot, tired, fatigued and 
disinclined to work, and has some headache. It is noteworthy that, 
despite all these symptoms, the appetite for the evening meal is not 
diminished, which is not, as a rule, observed in fever due to other 
causes. Anorexia is a constant accompaniment of fever, excepting the 
fever of early phthisis. This tolerance of fever by the tuberculous mani- 
fests itself also in their aptitude to work during the day, and sleep 
during the night as if they were well, feeling only somewhat tired or 
languid, when the thermometer reads 101° F., or more. Finally, 
during the night more or less sweating may occur, which even in early 
cases may be so profuse as to drench the patient. 

Subjective Fever without Elevation of Temperature.— hese symptoms, 
in varying degrees of severity, are only rarely absent in incipient 
phthisis, and they are excellent guides in our attempts at excluding 
rises in temperature due to other causes. In fact, the afternoon languor 
just mentioned is so characteristic of the toxic state of the tuber- 
culous that we often meet it in some advanced cases—notably, fibroid 
phthisis—which are afebrile. In such cases we may speak of subjective 
fever without elevation of temperature, first described by Dettweiler. 
I have seen it in a few cases of incipient tuberculosis. For this reason 
we must not rely solely on thermometry while treating tuberculous 
patients. Conversely, fever without subjective symptoms is occasion- 
ally, though very rarely, seen in incipient cases and the prognosis is 
very good indeed. 

Provoked Fever.—The heat center is apparently easily disturbed 
in phthisis and as a result we have usually a labile, or unstable, tem- 
perature. Conditions which in the average normal individual have 


1 Tuberculose Pulmonaire, Paris, 1905, p. 59. 


219 


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220 FEVER AND NIGHTSWEATS 


no effect on the temperature may elevate it in the consumptive. Thus, 
a heavy meal, moderate exertion, emotional disturbances like reading 
or writing a letter, worry, anxiety, and excitement, especially during 
the early morning hours, may raise the temperature from 1.5° to 3° F. 
and more. I have seen the excitement of a medical examination raise 
the temperature of a patient in my office 3.5° within one-half hour, and 
in European sanatoriums it is a routine measure to inject water at 
the beginning of a course of tuberculin treatment with a view of ascer- 
taining whether the febrile reaction is really due to the tuberculin or 
to emotional disturbances. On visiting days in sanatoriums a large 
proportion of patients have higher fever than on other days. It has 
also been observed that a change in residence, as the admission into 
an institution, a railway journey, giving a sanatorium patient leave 
to spend a day with his family, etc., may elevate the temperature of 
the consumptive. 


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Fic. 37.—Female, aged nineteen years. Premenstrual fever in an afebrile case of 
incipient tuberculosis. (Bray.) 


This fiévre provoquée, first described by Daremberg, and then again 
by Penzoldt,! can be utilized for diagnostic purposes in cases sus- 
pected of incipient phthisis. When we have a patient presenting 
indefinite symptoms and signs of tuberculosis, but the temperature 
is normal, we may take the temperature before and after active exer- 
cise, and if it is raised 1° F. or more, we are probably dealing with a 
case of incipient tuberculosis. The usual rule is to let the patient 
walk about two miles and note the effect. My way has been to ask the 
patient to take his rectal temperature before he starts out for my 
office, and then walk one and a half or two miles while coming. Im- 
mediately on his arrival his temperature is again taken, preferably 
with the same thermometer. 

A rise of 1° or more in the temperature after such a test is highly 
suggestive of tuberculosis. Daremberg insists that it is conclusive. 
Combined with other symptoms and signs, it is undoubtedly of great 
value. But in obese persons this may be observed without any tuber- 


1 Handbuch der Therapie, Jena, 1910, 3, 188. 


FEVER 221 


culous lesions in their lungs and the same is true of anemic, especially 
chlorotic young women, and in individuals with focal infections in any 
location—the gums, sinuses, Fallopian tubes, etc. But in physiological 
rises after exercise the elevated temperature again sinks to normal 
within half an hour of rest, while in the tuberculous it lasts much longer, 
two hours, or even more. 

Menstrual Fever.—In women the fever may be more accentuated 
during the menstrual period, which at times is of diagnostic importance 
(Fig. 37). We must, however, remember that in many non-tuberculous 
women slight elevations of temperature are observed a few days before 
or during that period. But in the phthisical we meet not only with 
elevation of temperature, but occasionally also with an increase in the 
number of rales over the site of the lesion, hemoptysis, and pleuritic 
pains. Macht! says that “the rise in temperature may occur in afebrile 
patients, that is, patients who ordinarily run no fever, as well as in 
those who run a slight temperature throughout the month. These 
rises may occur in early cases as well as in advanced, and in the former 
are of considerable diagnostic importance. If a patient shows a con- 
stantly recurring menstrual rise in temperature, and pelvic disease 
cannot be found, a tuberculous process should always be borne in 
mind.” 

In most cases the fever declines with the appearance of the flow; 
it may last several days, or only a few hours. Sabourin? has shown that 
in certain women the menstrual fever lasts three weeks and leaves the 
patient only one week before the onset of the next menstruation. In 
these cases it is of grave importance; the patients “are killed by their 
courses,” as Sabourin says. 

Many authors, notably Vandervelde, Sabourin, Wiese,’ C. A. Welch,! 
E. C. Morland,’ and others, state that premenstrual fever indicates 
latent or active tuberculosis and should be given attention when 
attempting to make a diagnosis in doubtful cases. This premenstrual 
fever occurs a few days before the onset of menstruation and may 
continue throughout the days of the flow. Considering that it has been 
found that in from 40 to 50 per cent of tuberculous women there is 
hyperthermia before and during that period, while in healthy women 
the percentage is considerably less, these authors maintain that it is of 
considerable diagnostic value, and that the absence of menstrual fever 
excludes active tuberculosis. 

According to Macht, these rises in temperature, when reaching 
high, are an evil omen prognostically; on the other hand, if they grow 
less, or disappear altogether, it is a sign of a cured, or an arrested 
condition. 

Evaluation of Fever in Tuberculosis.—In the usual case of chronic 
phthisis in the incipient stage there is a subfebrile temperature which 


1 Am. Jour. Med. Sci., 1910, 140, 835. 2 Rev. de méd., 1905, 25, 175, 
3 Beitr. z. Klin. d. Tuberk., 1912, 26, 335.' 
4 Lancet, 1910, 1, 639, 5 Tbid,, 821. 


222 FEVER AND NIGHTSWEATS 


is often overlooked, unless the thermometer is used every two hours 
for a week or two. The feeling of languor which overtakes the patient 
during the afternoon is often taken as an indication of neurasthenia, 
the anorexia is attributed to dyspepsia, and the real cause overlooked. 
From Fig. 38 it will be seen that if in this case the temperature had 
been taken only at 8 A.M., 12 M., and 8 P.M., as is usually done, the 
febrile reaction at three to six would have been overlooked, and the 
patient pronounced afebrile. In rare cases, these febrile reactions occur 
during the night and thus escape detection. Still rarer is the so-called 
“reversed type”’ of fever, the febrile reaction occurring during the early 
morning hours. It appears that the prognosis is unfavorable in the 
last class of cases. 





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Fic. 38.—Incipient phthisis, active lesions in left apex. Temperature taken every 
three hours (black line) shows daily exacerbations of the fever reaching 102° F. in the 
afternoon. This exacerbation would be missed if temperature was only taken three 
times a day, at 8 A.M., 12 M., and 7 p.m., as is shown by dotted curve. 


Since a subfebrile temperature for one or two days is no conclusive 
proof of the existence of active phthisis, because such ephemeral 
hyperthermia may be due to other causes, and also because there 
are afebrile days during the incipient stage of phthisis, the temperature 
should be taken continuously for two or three weeks in doubtful cases 
before arriving at a conclusion. The readings thus plotted on the 
chart are the best graphic criteria for diagnosis. 

The slight afternoon rises in temperature characteristic of incipient 
phthisis are not exclusively met with in this disease; there are other 
conditions which may produce hyperthermia for weeks, greatly sim- 
ulating phthisis. For this reason we must not hastily decide in favor 
of this disease unless there are other symptoms and signs of lung 
disease. I have had under my care a woman who was treated for 
several months in a sanatorium, then handed over to surgeons for opera- 
tion for gall-stones, and while convalescing after the operation another 
diagnosis of tuberculosis was made. The woman was then admitted 
to the hospital under my care and for three months the afternoon 
temperature was almost invariably elevated 1° to 3°. We finally gave 


FEVER 223 


her work as a nurse and she worked during the succeeding six months 
quite hard and has not developed phthisis, nor shown any indications 
of the disease on physical exploration of the chest. I knew several 
individuals who had subfebrile temperature almost every afternoon, 
yet no cause could be found; however, they continue healthy. These 
afternoon rises in temperature, when not due to tuberculosis, are mainly 
found in women. Anemia, especially chlorosis, and occasionally per- 
nicious anemia, may be the cause. However, an examination of the 
blood clears up the case. Purulent conditions of the nose and acces- 
sory sinuses, pyorrhea, chronic inflammatory conditions of the tonsils, 
chronic otitis media, non-tuberculous bronchiectasis, pyelitis, diseases 
of the female genitalia, cirrhosis of the liver, hyperthyroidism, syphilis, 
Hodgkin’s disease, pernicious anemia, leukemia, malignant neoplasm 
of the lungs, ete., may be accompanied by subfebrile temperature. 
These are but a few of the conditions which must be looked for in 
doubtful cases. 

After all, purely hysterical fever must be borne in mind when 
everything else has been ruled out. There is no question but that it 
does occur, although our modern views of the pathogenesis of fever 
are against it. This appears to be one of the many paradoxes in 
clinical medicine. 


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Fie. 39.—Fever in incipient tuberculosis. Temperature taken every three hours. 


In evaluating the significance of the temperature range in active 
phthisis, we may be guided by the rules laid down by Harris and L eale:! 
The higher the day temperature, the more active the disease, except 
in a few rare instances (the so-called “reverse type’’) where the ordi- 
nary fluctuations are reversed, and the evening temperature remains 
lowest throughout the whole course of the disease. Eut whether the 
normal or the inverted remissions take place, the lowest temperature 
is always above normal, and so long as it follows this course, it may be 
assumed that active deposition of tubercle is taking place, even though 
the physical signs remain for the time unaltered. 

Most patients with fever lose in weight, but there are many excep- 
tions, and patients as well as physicians are apt to judge a case more 


1 Treatment of Pulmonary Consumption, London, 1895, p. 314. 


224 FEVER AND NIGHTSWEATS 


by the scale than by the thermometer. This is wrong. There are cases 
of phthisis, especially those in whom the fastigium occurs during the 
night, that remain stationary or gain in weight, while the process in 
the lungs keeps on progressing. In other words, neither fever nor 
the weight alone should be taken as a criterion for prognosis, but all 
the concomitant symptoms and signs should be considered in this 
connection. 

On the other hand, the absence of pyrexia, while a good sign in 
most cases, is not conclusive evidence of the mildness of the process, 
especially when other symptoms of active disease are present. I 
have seen many patients in whom the temperature never exceeded 
101° F., or was even less, still the anorexia, emaciation, cough, hemop- 
tysis, etc., were all active in bringing them to a fatal termination. 
This is especially seen in cases which have lasted for some years. The 
organism has adapted itself to the disease and does not react any 
more to the same degree that it does usually, and its defensive forces 
are in abeyance. It may be observed in patients with any lesion, not 
excluding those with large, but usually dry, cavities in the lungs. 






































































































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Ira. 40.—High, continuous fever in the terminal stages of pulmonary tuberculosis. 


Types of Fever in Chronic Tuberculosis.—In progressive and also 
in advanced cases of phthisis the fever is not typical, and a diagnosis 
cannot be made from an analysis of the temperature curve alone, as 
is often the case in malaria, relapsing fever, typhoid, pneumonia, ete. 
In phthisis we may meet with any type of hyperthermia in different 
patients, and in the same patient at different times, depending on the 
activity of the process, mixed infection with pyogenic organisms, soft- . 
ening of lung tissue, free drainage of necrotic foci, mobilization of tuber- 
cle bacilli into the blood stream, etc. Very frequently we note in the 
same patient different. types of fever at different times, and passing 
into the other suddenly or gradually. Under the circumstances we 
cannot speak of a typical tuberculous fever, But we meet with certain 


FEVER 


temperature curves which, at times, 
serve as good and reliable guides in 
our attempts at ascertaining the con- 
dition of the patient, the presence or 
absence of complications, and espe- 
cially when attempting to formulate a 
prognosis. 

Continuous Fever.—This is met with 
especially in cases with extensive pneu- 
monicinvolvement, in acute pneumonic 
phthisis, in tuberculous bronchopneu- 
monia in children, and in acute miliary 
tuberculosis. Inchronic phthisis which 
has pursued a favorable course, when 
a continuous temperature develops 
after a pulmonary hemorrhage, or 
without any visible cause, we may con- 
clude that there has occurred an exten- 
sion of the process in the lungs; and if 
this high, continuous temperature— 
even when it does not exceed 103° F. 
—lasts more than three or four weeks, 
the prognosis is very grave and a 
fatal issue may be looked for. In some 
cases a slight improvement may occur, 
but it is noteworthy that they are never 
cured. Combined with dyspnea, cyano- 
sis, and prostration it is an indication 
of miliary tuberculosis, which is a fre- 
quent terminal phenomenon in chronic 
phthisis. 

Cyclic Fever.—In many cases of 
chronic phthisis we meet cyclic or un- 
dulating types of hyperthermia. The 
patient is never free from fever, but 
for two or three days during the week 
the maximum reading reaches 102.5° 
or 103.5° F., or even more, while the 
other four or five days it ismuch lower 
—100.5° to 101.5° F. These wave-like 
fluctuations may appear more or less 
periodically for months and not only 
show variations during each week, but 
the febrile waves may appear at greater 
intervals, every two or three or four 
weeks, as can be seen from Fig. 41. It 
is seen in cases in which old foci are 

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Fie. 41.—Active tuberculosis with continuous fever, marked by acute exacerbations, occurring at irregular intervals. 


226 FEVER AND NIGHTSWEATS 


softening, or the pulmonary process is extending, and each exacerbation 
of the fever is an expression of a new area of involvement which may, 
in many cases, be easily discerned by a careful physical exploration of 
the chest. The diagnostic and prognostic significance of undulating 
fever in pulmonary tuberculosis has recently been treated in detail 
by R. Burnand.! 

Hectic Fever.—In progressive disease these types of hyperthermia 
are usually followed at the end by hectic fever (Fig. 42). In cases in 
which there is softening in the lung, the necrotic tissue being gradually 
expelled leaving cavities, the temperature chart tells the story. There 
are morning remissions during which the temperature is nearly normal, 
or even subnormal, while in the afternoon there may be a chilly sensa- 

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Fic. 42.—Hectie fever in advanced cavitary phthisis. 


tion, or a distinct chill, with chattering of the teeth; the pulse, which 
was rapid and small during the apyrexial morning hours, is even more 
accelerated, the temperature begins to rise, reaching 103°, and in some 
cases even 105° at about five in the afternoon. The nightsweats in 
these cases are very profuse and exhausting. 

The time of the highest fever in these hectic cases is variable. Often 
the maximum is attained in the afternoon, but in many it is around 
noon, and in the evening it may be normal. If in such cases it is taken . 
only mornings and evenings, we may find a record of normal tempera- 
ture, because the midday rise, which may have been quite high, has 
been overlooked. 

This hectic fever may last for weeks, or even for months, during 


1 Ann. d. méd., 1919, 6, 110. 


FEVER yyH' 


which time the unfortunate patient is reduced to a skeleton by the 
fever and the accompanying anorexia and diarrhea, which are hardly 
ever lacking. The frightful appearance of the bundle of bones with 
hardly any visible muscles, which have atrophied extremely, covered by 
a clammy, muddy skin; the skin emaciated but edematous around the 
ankles and knees; the lips and fingers cyanosed, the eyes deeply set 
in the orbits, the temples sunken, are disheartening to the physician 
making his rounds in the hospital; he feels helpless when the slowly 
sinking, but still struggling, human being gazes, appealing for assist- 
ance which cannot be given. It is noteworthy that with all this material 
decay the intelligence, and often the hopes and aspirations of the 
patient, are well retained, and he begs for the relief of some minor, and 
comparatively insignificant symptom, such as the cough or diarrhea, 
saying that if this is removed he will feel in excellent condition; many 
beg to be sent to some distant clime where they are sure of a cure. 


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Fria. 43.—Irregular fever in advanced tuberculosis of the lungs with intestinal 
complications. 


At the terminal stages there may be irregular fever; the curve of 
one day differs from that of the other. Saugman! states that this is 
a good sign of intestinal tuberculosis when occurring in the earlier 
stages of the disease (Iig. 43). 

Subnormal Temperature —The subnormal temperature seen in many 
incipient cases during the morning hours has already been mentioned. 
But we also meet with patients in the advanced stages of the disease 
who present subnormal temperature throughout the day and night 
for weeks; the mercury never rises above 98.5° F., and early in the 
day it may be as low as 96° or 97° F. The disease may be active and 
even progressive, yet the thermometer gives no indication of it. I have 
had many of these cases in my hospital service. I find it is usually 
an indication of excavation, just as fever is an indication of infiltration, 
caseation, and softening of lung tissues. 


1 In Brauer, Schréder and Blumenfeld’s Handbuch der Tuberkulose, 2, 284. 


228 FEVER AND NIGHTSWEATS 


Subnormal temperature is also seen in fibroid phthisis, and in 
emphysema complicated by tuberculosis, in both of which the disease 
runs a chronic, sluggish course. Many keep disabled for years, though 
not confined to bed, but they never fully recover. A subnormal tem- 
perature is also seen on rare occasions in a subacute case of phthisis, 
which suddenly takes a turn for the better after the necrotic tissue in 
the lung has been eliminated from that organ and a cavity remains. 
In this class recovery may take place, as I have seen in several instances. 

A sudden drop in the temperature, combined with dyspnea and 
cyanosis, in a febrile case of phthisis may mean a spontaneous pneumo- 
thorax, or a rapid extension of the necrotic process in the lung over- 
whelming the patient or, rarely, complicating and terminal miliary 
tuberculosis. The prognosis in either event is grave indeed. In many 
extremely emaciated consumptives the temperature is at times sub- 
normal for several days before death and this does not exclude miliary 
tuberculosis. 

Apyretic Tuberculosis.—In old -chronic cases of phthisis we may 
have a normal temperature for months, though the process in the 
lungs keeps up. This is seen in fibroid phthisis, in phthisis in the aged, 
and in tuberculous pleurisy. Many of these patients live for years and 
do not lose in weight. I have seen such patients last for fifteen and 
twenty years, always ailing, coughing, expectorating, at times hav- 
ing spells of more or less profuse hemoptysis. They are important 
sources of the dissemination of tubercle bacilli; more so than most 
of the stormy cases. They are not strong enough for muscular work, 
but may be moderately efficient at any occupation which does not 
require undue exertion. We meet these cases mainly among the well- 
to-do, who can afford to lead an idle life, or among the very poor who 
have intrenched themselves in hospitals for chronic and “incurable” 
cases of tuberculosis and, for one reason or another, like institutional 
life, and stick to it for long periods. We also meet these active, but 
apyretic, cases among the more cultured classes, who either know how 
to take care of themselves or, being professional persons, they pursue 
their vocations, which do not involve muscular exertion, with more or 
less efficiency. Some are very brilliant, and the type of consumptive 
drawn by so many writers of fiction is usually copied after the model 
of this class of patients. It is noteworthy that while most of them are 
more or less emaciated, we now and then meet one who is actually 
fat, and may even be placed in the category of the obese. They usually 
suffer from dyspnea, because of the fatty heart and pulmonary fibrosis. 

Phthisis in the aged also runs an apyretic course at times and, because 
they do not cough excessively, the disease may not be recognized. 

It appears that there are great differences in the reactive powers 
of different persons suffering from phthisis. In some the fact that 
they have normal temperature is no proof that the disease is benign, 
especially if other symptoms of active disease are present. I have 
seen patients whose temperatures hardly ever exceeded 101° F., yet 


FEVER 229 


they wasted, perspired, and had exhausting diarrhea; they finally 
died with a low temperature. While the temperature curve is an 
excellent guide as to the tendencies and progress of the disease, these 
apyretic cases must be judged more by the general symptoms and the 
physical signs than by the thermometrical findings, as has already 
been shown. 

Fever Due to Complications.—During the course of phthisis fluctua- 
tions in the temperature usually go hand-in-hand with the activity 
of the disease, and each elevation or depression in the temperature 
curve may be explained by the findings in the chest through physical 
exploration. But there are exceptions. Many elevations of the tem- 
perature are due to non-tuberculous complications. Thus, as will 
be seen from Fig. 44, malaria may complicate phthisis and create 
confusion, unless the blood is examined and the malarial parasite is 
found. 

Other complications to be mentioned are constipation, acute gas- 
tritis, tonsillitis, influenza, pleural effusions, etc. These may be the 
cause of a sudden elevation of temperature in a case in which the 
tuberculous process is proceeding rather favorably. Careful examina- 
tion usually reveals the cause of the pyrexia. 

A rise in the temperature in a tuberculous patient may be due to 
the administration of certain drugs, mostly of the sedative and hyp- 
notic class, as has been pointed out by Sabourin! and Mantoux.? The 
writer has repeatedly observed that after the administration of opium, 
or its derivatives, morphine, codeine, heroine, dionine, etc., or chloral, 
veronal, sulfonal, trional, etc., there is a rise in the temperature during 
the succeeding twenty-four hours. A rise of this kind is especially vivid 
when occurring in an afebrile patient to whom one of these drugs has 
been administered. The fever lasts no more than twenty-four hours, 
as a rule, but I have seen cases in which it lasted longer. Hypodermic 
medication is more apt to act this way, and injections of salt solution 
may also elevate the temperature. 

Diagnostic and Prognostic Significance of Fever in Phthisis.—Sum- 
marizing the results obtained in this section, we may say that in a 
patient who shows a distinct elevation of temperature during the afternoon 
for several weeks, and no other cause can be found, tuberculosis is to be 
thought of. If it is provoked by moderate exercise, and persists after 
more than an hour of rest, it is almost pathognomonic of phthisis. If 
with it there are other symptoms, such as nightsweats, languor, loss 
of weight, cough, emaciation, etc., tuberculosis is in all probability 
the cause, even if the physical signs are not definite. The diagnosis is 
more certain if the morning temperature is subnormal. 

Instability of the temperature and pulse is found in nearly every 
case. But it is not pathognomonic of tuberculosis. Overexertion will 
raise the temperature in every individual with a focal infection of any 


1 Rey. gén. de clin. et de thérap., 1906, 20, 639. 
2 Rev. de la tuberc., 1907, 4, 395. 


230 FEVER AND NIGHTSWEATS 


kind in the body. Moreover, any aberration of the sympathetic or 
endocrine system may be accompanied by instability of the pulse and 
temperature. This is especailly true in cases of hyperthyroidism. 
The fact that this is often accompanied by other general symptoms 
simulating tuberculosis—tachycardia, emaciation, cough, sweating, 
malaise, fatigue, ete.—makes it more difficult at times to differentiate 
the two conditions. The effects of nervous tension, anxiety and sus- 
pense have been spoken of above. 


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Fia. 44.—Malaria complicating phthisis. 


In the course of the disease a high temperature during the day, never 
touching the normal, and ascending in the evening is an indication of 
progressive activity of the process in the lung. The disease is progressing 
slowly, or is even quiescent, when the temperature in the early morn- 
ing on rising is subnormal or normal and remains so during the day, not 
rising above 101° F. late in the afternoon or evening. 

High, continuous temperature, above 103° F., is an indication of 
extension or dissemination of the disease in the lung, and if it lasts for 
more than a month, a fatal issue is to be expected; even if some 
improvement is noted, recovery should not be expected. 

Hectic fever, with normal or subnormal temperature in the morning, 
and high fever, 103° or more at midday or later, 1s an ill omen. While the. 
patient may keep on in this condition for weeks or months, he will in 
all probability never leave his bed alive. 

In most cases, absence of fever is an indication of an improvement or 
a cure of the disease, but there are many exceptions, and the other con- 
stitutional symptoms must be considered when formulating a prognosis. 


NIGHTSWEATS 231 


A subnormal temperature, when coming on suddenly, is a bad sign. 
When chronic, lasting for several weeks, however, it is not incompatible 
with an inefficient, though not necessarily an inactive, life. 


NIGHTSWEATS. 


Nightsweats have at all times been considered pathognomonic of 
phthisis. A prolonged cough will not alarm the average person, but 
when it is associated with nightsweats, he will soon consult a physician 
with a view of ascertaining whether or not he is tuberculous. They 
are met with quite early in the disease in many cases; at times when 
the characteristic symptoms and physical signs are lacking, but in 
advanced cases their severity does not depend altogether on the extent 
of the lesion. 

Causes.— The causes of nightsweats are obscure. Traube attributed 
this phenomenon to the compensatory activity of the skin when the 
pulmonary respiratory area is diminished, but we meet them in cases 
with but little damage to the lung. Gustav Heim! is of the opinion 
that the products of cell disintegration, and especially the toxins pro- 
duced by the bacilli, stimulate the sweat center directly or reflexly, 
just as after childbirth the remains of the placenta may produce 
sweating. It is an attempt on the part of the body to rid itself of 
harmful matter, as it is excreting carbon dioxide in the sweat when this 
is excessive in the blood. Smith and Brehmer have attributed the night- 
sweats to the quick change of the tachycardia of the day to the brady- 
cardia of the night. It is more rational to see in nightsweats a result 
of the decline of the high temperature in the afternoon and evening 
to the low temperature of the remission during the early morning 
hours. This phenomenon is seen during, and soon after, the crisis in 
many other febrile diseases. The diminution in the pulse-rate and in 
the blood-pressure, owing to the atony of the bloodvessels, especially 
those of the skin, favors sweating and assists in ridding the body of 
the toxins. 

Cornet looks upon nightsweats as due to the absorption of the proteins 
of the tubercle bacilli and other microdrganisms secondarily implanted 
in phthisical lesions. The toxins are absorbed into the blood stream 
and they stimulate the heat center, thus causing fever; and also act 
upon the sweat center in the cord and medulla and the peripheral 
secretory glands and thus produce perspiration. He shows that this 
also confirms the fact that, in spite of the great disturbance, the dimin- 
ished excretion of fluid, and the greater difficulty in the elimination 
of carbon dioxide which is characteristic of the chronic course of the 
disease as compared with acute phthisis, the secretion of sweat is 
incomparably less in the former, owing solely to the more gradual 
absorption of the toxins. 


1 Ztschr. f. Tuberk., 1910, 16, 365. 


232 FEVER AND NIGHTSWEATS 


Symptomatology.—Nightsweats usually occur in the second part of 
the night, about 2 to 4 A.M., in typical cases. The patient retires with 
some fever, and in hectic cases may have had a chill on the preceding 
afternoon, sleeps rather restlessly, is disturbed by dreams or by cough, 
and wakes up during the early morning hours drenched with perspira- 
tion. At times, changing the night- and bedclothes may prevent their 
recurrence during the same night, but in many cases this is of no avail, 
as the sweats again trouble the unfortunate victim. 

In the milder forms, the sweating may be local, on the forehead, 
the neck, the chest, etc. Rarely it is noted on only one side of the body, 
usually the one corresponding to the pulmonary lesion. 

In the progressive and hectic cases the sweating may be so profuse 
and drenching as to exhaust the patient, who often begs for the relief 
of this symptom alone which, together with the diarrhea, is instru- 
mental in relieving him permanently from his earthly sufferings. 

It is important to mention that the nightsweats do not directly harm 
the patient, considering that only 1 per cent of solids is eliminated in 
this way, of which 0.7 per cent is salts, mainly uric acid. Only so far 
as disturbing sleep is concerned are nightsweats harmful. In children 
their diagnostic significance is less than in adults. (See Chapter 
XXIV.) 

In some cases the disease runs its course without any, or only with 
slight nightsweats. Kuthy found that 37 per cent of his patients had 
nightsweats during the first stage of the disease. In the third stage, 
61.5 per cent. According to this author, women are more apt to sweat 
profusely than men. But Louis found only 10 per cent of cases with- 
out nightsweats, and at the Phipps Institute they were absent in 41 
per cent of 3344 cases. 

In the evolution of phthisis it is observed that, as a rule, the sweats 
run hand-in-hand with the fever and the general condition of the 
patient. During afebrile periods they are absent to return with an 
acute exacerbation. There are said to have been observed cases of 
nightsweats without fever, but my experience leads me to believe that 
the fever was overlooked in such cases. One of the best signs of improve- 
ment is the complete disappearance of the nightsweats. 

Nightsweats may be prevented in a large proportion of cases by 
the adoption of hygienic bedding and coverings during sleep, as will 
be shown in another part of this book. 

Sweating appears to be easily provoked in the phthisical. Kuthy 
and Wolff-Eisner say that not only consumptives, but also those 
“predisposed” sweat easily, who, when waking, find themselves bathed 
more or less in perspiration. Mild exertion, grief, worry, excitement, 
etc., may be followed by more or less profuse perspiration, general or 
local. In a large proportion of patients we see sweating in the armpits 
during medical examination, even in patients who do not sweat during 
the night. We also meet with patients who sweat during the day while 
taking a nap, ete. 


NIGHTSWEATS 233 


While most authors, notably Cornet, state that the sweat does not 
carry infection, investigations by Piéry have shown that it may 
contain bacilli which are pathogenic to animals. However, this has 
not been confirmed by other investigators. Probably the sweat col- 
lected by Piéry was contaminated by bacilli after it was secreted. 
Salters showed that hypodermic injections of the sweat into animals 
act like tuberculin, which may be expected, considering that it assists 
in eliminating tuberculous toxins from the body. 


CHAPTER X. 
HEMOPTYSIS. 


Frequency.— To the layman the most reliable symptoms of pul- 
monary tuberculosis is blood-spitting and many physicians share this 
view, although we know that a large proportion of cases of phthisis 
pursue their course and terminate in recovery, or fatally, without any 
hemoptysis, while in many patients hemoptysis is not due to tuber- 
culosis. The statistics of the frequency of this symptom vary con- 
siderably, some finding it in but 25 per cent, while others report as 
many as 80 per cent having had hemorrhages during the course of 
phthisis. Sokolowski says that advanced consumptives who did not 
bleed from time to time are only rarely met with. Louis found this 
symptom in 65 per cent of cases; Walshe! in 80 per cent; Wilson Fox? 
says that more than one-half of all cases of phthisis present this symp- 
tom in some part of their course; Williams found it in 70 per cent; 
Sorgo* in 38 per cent; Condie in only 24 per cent; Elmer H. Funk 
among 373 patients with advanced disease, in 44 per cent; among 
167 patients traced to the end in 54 per cent, and at the Phipps 
Institute at Philadelphia, it was found in 49.9 per cent of 4466 tuber- 
culous patients. 

These wide differences in the percentages are easily explained by the 
fact that the authors have not taken their figures from comparable 
material. Some have spoken only of fatal cases, others of cases in their 
private practice, while still others have taken hospital records as their 
criteria. In the latter classes the patients were observed only for a 
short time, and hemorrhages which may have taken place later have 
not been considered. 

Anders‘ found in a series of 5302 cases that 36.6 per cent had hemop- 
tysis. He emphasizes, however, that not all were followed until the 
death or recovery of the patients, but many were discharged during 
the course of the affection. In fact, among 289 cases in private prac- 
tice, kept under observation for a longer time, as a rule, hemoptysis 
occurred jn 41.8 per cent, but it is to be recollected that even these 
patients were under observation for less than half of their duration. 
Hemorrhage is more apt to occur in advanced cases, and those who 
base their calculations on early cases in sanatoriums are likely to find 
low percentages, while when only fatal cases are taken the percentages ~ 
will be too high. 


1 British and Foreign Med. Chir. Review, 1849. 

2 Diseases of the Lungs and Pleura, London, 1891, p. 785, 

3 In Brauer, Schréder and Blumenfeld’s Handbuch d. Tuberkulose, 2, 250. 
4 Jour. Am. Med. Assn., 1907, 49, 1067; 1909, 53, 455. 


PATHOLOGY 239 


Pathology.—The diagnostic and prognostic significance of hemop- 
tysis can only be appreciated when we have a clear understanding 
of the anatomical changes responsible for the bleeding. There are 
several varieties of pulmonary lesions which may bring about extrava- 
sation of blood from the lung tissues: Local inflammatory or active 
hyperemia; ulceration of a bloodvessel, and aneurysmal dilatation of 
bloodvessels are the most important in phthisis. 

The initial hemoptyses are said to be caused merely by localized, 
active inflammatory hyperemia. In other words, they are of the same 
origin as the rusty sputum of pneumonia and the hemorrhages in 
influenzal bronchopneumonia. This bleeding, caused by diapedesis 
and active congestion of the pulmonary parenchyma, may be profuse, 
though in most cases only blood-streaked sputum is thus brought out. 
On the other hand, blood-streaked sputum does not invariably mean 
that it is caused by localized hyperemia and that the lesion is not 
serious, because not all the extravasated blood is brought out through 
the mouth. Quite some of it remains in the lungs and bronchi, and is 
more or less quickly absorbed, as was shown by Nothnagel. When 
the hemorrhage 1s not profuse we must not conclude that the case is mild, 
or that the lesion is not eatensive. 

When the pulmonary lesion proceeds from infiltration to caseation, 
then to softening, and finally to liquefaction, it undoubtedly implicates 
the bloodvessels that pass through it and produces in them the same 
changes as in the lung tissue. It is therefore strange at first sight that, 
considering the ulcerative processes and the destruction of tissue, 
hemorrhages do not occur more often. But this is explained by the 
strong tendency to the formation of thrombi in the bloodvessels, except- 
ing in very acute cases. In chronic cases there usually occurs a narrow- 
ing, or complete obliteration, of the veessl by the growing tubercles 
which, when finally ulcerating, may leave an erosion through which the 
blood can flow more or less freely until it is occluded by a thrombus. 
Moreover, the increased blood-pressure at the infected and inflamed 
area dilates the softened vessels, and causes small aneurysms, the 
aneurysms of Rasmussen, which have been described elsewhere (see 
p. 176). This is clear when we bear in mind that the bloodvessels 
in the lungs are terminal branches of the pulmonary artery. 

Most cases of hempotysis end in recovery, and the pathological 
changes in the lung at the time of the bleeding can only be surmised, 
but in fatal hemorrhages we often have an opportunity to observe the 
anatomical changes. Here we usually find that the source of the 
bleeding was an exposed vessel, left bare after the surrounding pul- 
monary tissue had softened and was eliminated. The loss of support, 
as well as the pathological changes in the perivascular tissues, and the 
erosions of the tunice adventitia and media, lead to aneurysmal dilata- 
tions of the inner coat which give way to the pressure exerted on them 
by the circulating blood. 

The rupture of these aneurysms at times strikes down a patient 


236 HEMOPTYSIS 


who is on the road to recovery when a hemorrhage occurs like a storm 
out of a clear sky. When the cavity into which the aneurysm, or the 
lacerated artery, opens is small, the extravasated blood usually coagu- 
lates, and the clot obstructs the opening of the bloodvessel, thus stop- 
ping the bleeding. But in large cavities, or when the blood is deficient 
in coagulability, which is not rare, the bleeding keeps on until the 
patient dies of acute anemia. I have seen at autopsy a large cavity 
filled with about a quart of blood which killed a patient during the 
night. After clearing out the clots we found an eroded artery about 
2 mm. in diameter, and passing a probe through it, we found it only 
about 6 em. from the pulmonary artery. This patient had such a sharp 
hemorrhage that he was unable to call for assistance. 

In more acute cases of phthisis, in which the destruction of lung 
tissue is going on at a rapid pace, the hemorrhages usually come from 
ulcerating erosions of large pulmonary vessels and may prove fatal 
immediately. Here there is no time for narrowing of the bloodvessels, 
thus preparing it that in case of rupture it may be easily repaired by 
occlusion with a thrombus which saves the majority of chronic con- 
sumptives from death due to this cause. In acute pneumonic phthisis, 
which very often begins with sharp and profuse hemorrhage, I have 
usually been able to find signs of cavitation when the acute process 
subsided and the disease pursued a chronic or subacute course. This 
confirms the view that profuse hemorrhage is not caused by mere active 
inflammatory hyperemia, but by actual erosion of a bloodvessel. 

In fibroid phthisis the sources of hemorrhages are lacerated, dilated 
or varicose bloodvessels which pass through bronchiectatic cavities, 
characteristic of this form of the disease, and also oozing from capillaries 
or arteries which traverse the granulations on the walls of the cavities. 
The bleeding is therefore not profuse, as a rule, but it is recurring in 
many cases. 

Effects of Hemorrhage.—It has been found experimentally that 
animals can withstand the loss of one-half of the total amount of 
blood in the body. When death does ensue, it is not due primarily to 
the diminution in the number of red blood cells, but because of the 
sudden drop in the blood-pressure resulting from scanty filling of the 
bloodvessels and the heart. At first the bloodvessels contract and thus 
maintain the blood-pressure, but later they dilate and a proportional 
hypotension results. When the hemorrhage is not extremely copious 
and rapid, the bloodvessels are soon filled with fluid absorbed from the 
body juices. Therapeutically we attain the same end by transfusion. 
The result is that in acute primary anemia the pulse is rapid owing 
to the rapid heart action, but it is small owing to the oligemia. With 
excessive loss of blood cerebral anemia ensues. Fainting due to this 
cause has been observed when 500 ce of blood is rapidly lost; 1500 to 
2000 ee of blood rapidly lost from the body is fatal. In anemic tuber- 
culous patients, who have an oligemia even before the intercurrent 
pulmonary hemorrhage, even a smaller amount may end fatally. 


HEMOPTYSIS AT THE ONSET OF PHTHISIS 237 


Initial Hemoptysis.—Of great interest is hemoptysis as an initial 
symptom of phthisis. But statistics on this subject are also at variance, 
because we meet with many patients who have been coughing and 
presented other symptoms of tuberculosis for months, or even years 
and paid little attention to them until a hemorrhage brought them to 
their senses. Here it would not be correct to consider the hemoptysis 
as the first symptom. 

In a study of 1932 cases Reiche! found that 9.2 per cent had more 
or less profuse hemorrhage at the beginning of the disease, and in 
one-fourth of these it was rather copious. He finds that those who 
bleed at the beginning are more apt to bleed during the course of the 
disease than those who do not; the ratio is 57.9 per cent and 31.7 
per cent. Sorgo found during a period of observation extending over 
ten years that 12.9 per cent of 5872 patients had initial hemorrhages. 
Kuthy? reports that while 54.3 per cent of his patients had hemoptysis, 
only two-fifths of these (22.3 per cent) were initial hemorrhages. 
Anders arrives at the conclusion that in about 10 per cent of cases 
of phthisis, hemoptysis first directed attention to, and is almost invari- 
ably followed by, demonstrable and conclusive evidence of the disease; 
but in not less than 25 per cent of all cases of chronic pulmonary 
tuberculosis, hemoptysis is among the ushering-in symptoms of the 
active recognizable period of the affection. 

Hemoptysis at the Onset of Phthisis—As the first symptom to draw 
the attention of the patient to his affection, hemoptysis occurs in two 
different types. We meet it in patients who have felt perfectly well 
until the instant the hemorrhage made its appearance without any 
premonitory symptoms. Even close questioning does not elicit any 
symptoms preceding the bleeding. While at work, or engaged in an 
animated conversation, or even waking up from sleep during the night, 
the patient feels a sensation of warmth in the throat, coughs, and expec- 
torates a mouthful of blood; or during a fit of coughing he brings up 
some blood-streaked sputum. A careful examination of the chest and 
roentgenography may fail to disclose anything conclusive of pulmonary 
disease. The temperature is, and remains, normal, the appetite is good, 
but for a few hours or days the patient continues to bring up dark clots, 
and when this ceases he is apparently none the worse for his experience. 
Many of these patients subsequently pass through life without expe- 
riencing anything that may lead to the suspicion of tuberculosis. 
This is seen in those who have passed through an attack of abortive 
tuberculosis, details of which are given later on. Some patients give 
a history of such a hemorrhage many years before the onset of active 
phthisis. 

In others the initial hemorrhage continues for several days, and 
when it finally ceases the patient shows symptoms of phthisis—cough, 
expectoration, tachycardia, nightsweats, ete. Physical exploration 





1 Ztschr. f. Tuberk., 1902, 3, 223. 
2 Die Prognosenstellung bei der Lungentuberkulose, p. 299. 


238 HEMOPTYSIS 


of the chest reveals distinct signs of a lesion in one or both apices, 
and tubercle bacilli may be found in the sputum. The subsequent 
course of the disease is that of chronic phthisis, though a large propor- 
tion of cases are aborted within a few months, and I have met with 
patients who have had several attacks of hemoptysis at long intervals 
have shown some indefinite, or even conclusive apical signs, and rarely 
tubercle bacilli in the sputum, yet they remained well indefinitely. 

A different clinical type of hemoptysis is seen in patients who main- 
tain that they had felt quite well, but close questioning reveals the 
fact that they have been coughing for months, bringing up mucopuru- 
lent sputum; that the appetite has failed, and that they have lost 
weight and strength. In women we may find that they have missed one 
or more of their periods. They, however, considered these symptoms 
trifling, and continued at their work; or, consulting a physician, they 
were told that it was only a slight “cold.” 

The hemorrhage in these cases is apt to be profuse, and to last for 
several days because, while insidious in its arrival, the tuberculous 
process in the lungs has usually progressed quite far; indeed 1 have 
met with signs of pulmonary excavations in such “initial” hemorrhages. 
In the majority of cases physical exploration of the chest reveals a lesion 
of moderate extent, though on rare occasions we find nothing definite, 
even with the aid of roentgenography. But the cough, fever, night- 
sweats, expectoration, etc., continue, and the diagnosis is made with- 
out conclusive physical signs. In most cases tubercle bacilli are found 
in the sputum. It is the slow and prolonged convalescence after the 
attack of hemoptysis that distinguishes these cases from the initial 
hemorrhages of abortive tuberculosis. 

Hemorrhages during the Advanced Stages.—In confirmed chronic 
cases of phthisis we may meet with hemoptysis at any period of the 
disease, though it may be added that it is most frequent in the early 
and very late stages. The bleeding may be of various degrees, from 
that of sputum tinged with blood, to the expectoration of several 
mouthfuls of pure, bright red blood, to a copious hemorrhage during 
which several pints are brought up within twenty-four hours, and in 
rare cases it has been reported that as much as three quarts of blood 
were brought up. 

The blood is bright red, frothy, usually mixed with sputum. When 
bleeding is very profuse the blood may be “blue,” or venous. It is 
evident that in most cases the blood does not coagulate quickly— 
some clots are seen, but the bulk remains fluid; even the addition 
of calcium salts, serum and tissue extracts does not enhance its coagula- 
bility. E. Magnus Alsleben! has added normal blood without increas- 
ing its power of coagulation. The reasons for this delayed coagulability 
are not clear. 

Many patients have some premonitory warning before the onset of 


1 Ztschr. f, klin, Med., 1914, 81, 9. 


HEMORRHAGES DURING THE ADVANCED STAGES 239 


hemoptysis, and I have had one who could foretell bleeding twenty- 
four hours in advance. At times there is a rise in temperature, and 
pains in the chest are aggravated, or the cough becomes more annoying. 
But in most patients the onset is sudden and unexpected. The patient 
has a sensation of gurgling or tightness in the chest, followed by a 
fit of coughing productive of bright red, frothy blood which has a salty 
taste, and partly coagulates in the vessel into which it is deposited, 
forming flattened lumps. When very profuse, which is comparatively 
rare, the patient is overwhelmed and can hardly cough—the blood 
gushes in an almost steady stream through the mouth and at times 
through the nose. 

The general appearance of the average patient is that of shock— 
he is prostrated, often out of proportion to the amount of blood lost; 
his countenance is that of a frightened individual, unnerved, anxious 
and terrified; the face pale, the extremities cold and clammy. ‘The 
temperature, which may have been above normal before the onset of 
the bleeding, suddenly sinks, often to a subnormal degree; the pulse 
is rapid, soft, and small. 

That these symptoms of collapse are not due wholly to the loss 
of blood is evident from the fact that the family is also panic-stricken, 
and some are in the same state of collapse as the patient, showing the 
profound influence this symptom has on the average person. 

After getting some reassuring encouragement from his physician, 
there is usually observed a reaction in the patient—the pulse improves, 
the face becomes flushed, and the temperature rises to the same degree 
as it was before the onset of the bleeding, or higher. In many cases 
there is soon a relapse, the bleeding is repeated within a few hours or 
the next day, and it may keep on at irregular intervals for a week or 
more. When it finally stops the patient continues to expectorate 
dark blood-clots with his sputum for several days. In some cases the 
bleeding continues for weeks, letting up for a day or two, to reappear; 
rarely until the patient expires from exsanguination, cerebral anemia, 
and cardiac asthenia. 

In cases with large pulmonary cavities the bleeding may be very 
copious. The quantity of blood brought out is not all that has escaped 
from the bleeding vessel. A considerable part is swallowed automatic- 
ally, and some remains in the cavities or the bronchi, and is subse- 
quently absorbed. The outcome of the bleeding depends on the size 
of the bloodvessel which has eroded, and the coagulability of the blood. 
In rare cases the weak and emaciated patient is overwhelmed by the 
bleeding and is unable to expel it from the lungs, expiring in a few min- 
utes, drowned, or suffocated by his own blood. Other patients make a 
vain fight for hours, or days, but finally succumb to exsanguination. 
But the chances of recovery of a bleeding patient with a cavity in the 
lung are, on the whole, not bad. An immediate fatal issue vs, after all, 
exceptional; less than 2 per cent of bleeding consumptives die from hemor- 
rhage directly. he vast majority of hemorrhages are well borne, the 
patient dying, if at all, from other symptoms or complications, 


240 HEMOPTYSIS 


On the other hand, we meet with tuberculous patients who have 
made an excellent recovery, but suddenly profuse hemorrhages occur 
which carry them off within a few hours or days. I was once called to 
attend a patient who was discharged from a sanatorium three days 
previously as an arrested case of phthisis. He succumbed to the bleed- 
ing. ‘These hemorrhages are fortunately rare, and are usually due to 
the rupture of an aneurysm in a ‘“‘dry’’ and contracted cavity. They can 
neither be foreseen nor prevented. 

Hemorrhages in Fibroid Phthisis.—In this form of phthisis hemop- 
tysis 1s very frequent. In most cases it is very slight, only blood- 
tinged sputum being brought up. The patients may feel quite well 
in general, excepting for the dyspnea and the cough to which they 
have adapted themselves. But when blood make its appearance in 
the sputum they are alarmed. I have, however, had some patients 
who did not mind the blood-tinged sputum much, knowing from 
experience that it is not at all dangerous. Profuse and even fatal 
hemorrhages may, however, occur in fibroid phthisis. 

Hemorrhagic Phthisis.—There is a form of phthisis which is char- 
acterized by frequent and recurrent hemorrhages, the hemorrhagic 
phthisis of the old writers. The bleeding occurs at irregular intervals 
for years without harming the patient very much. In these patients 
we may not find any definite physical signs in the chest, no fever, no 
pronounced emaciation, and but little cough. Only the hemoptysis 
and, at times, the bacilli in the sputum reveal the condition. I have 
had under my care at the Montefiore Hospital a woman in whom neither 
any of the other physicians, nor myself, was quick in making a diag- 
nosis of tuberculosis from the indefinite physical signs and the roent- 
genogram of the chest. In fact, we had suspected malingering and 
employed strong measures to make sure that the temperature readings 
were not influenced by manipulations of the thermometer, and that the 
sputum was expectorated by the patient, suspecting that there was 
some deception on the part of the patient, who liked to remain in the 
hospital. Even during the more or less copious attacks of hemorrhage, 
which recurred at frequent, but irregular, intervals and often lasted 
for several weeks, no conclusive physical signs could be elicited in the 
chest. I have another patient who has bled at least twice a year for 
the past fifteen years and feels quite well. Andral mentions a patient 
who bled off and on for sixty years and finally succumbed at the age 
of eighty to some disease of the chest. These cases are uncommon 
but we meet them now and then. In some, we find signs of more or 
less extensive pulmonary lesions which remain stationary, or quies- 
cent, in spite of the recurring hemorrhages. ‘The lesion is benign. 
notwithstanding the tubercle bacilli which are found in the sputum, 
and at times, though rarely, there may be one hemorrhage which 
proves fatal. It has been stated that in most of these cases the lesion 
is localized in the tracheobronchial glands, but it is doubtful whether 
this pathology explains the recurring hemorrhages. 


EXCITING CAUSES OF HEMOPTYSIS 241 


Exciting Causes of Hemoptysis.— We have seen that while hemop- 
tysis is rather common among consumptives, still many pass through 
the disease until the end, recovery or death, without this accident. 
There appears to be some evidence showing that tall persons are more 
likely to bleed than those of shorter stature, and Wolff states that for 
this reason women show a lesser proportion of bleeders than men. 
Strandgaard! suggests that the tall patients are more likely to bleed 
because they have larger hearts and higher blood-pressure, but this 
view has not been confirmed. While hemoptysis has been seen at all 
ages, even in infants, still most of the cases occur between fifteen and 
fifty, probably because at this period most of the cases of phthisis are 
active. 

From Anders’s statistics it appears that males are more liable to 
hemoptysis than females, and prior to the twentieth year of age there 
is a slight preponderance in favor of the female sex. In Thompson’s? 
collective investigation the women showed greater liability than the 
men. But Anders shows that this increased incidence in the female 
sex is confined principally to the first two decades of life. After the 
thirtieth year the number of males preponderates. Females are also 
less liable to suffer from copious and fatal hemorrhages. My own 
experience coincides with that of Anders, that an immediately fatal 
hemorrhage is relatively rare in women. Initial hemoptysis is also less 
frequent in women than in men. Reiche’s statistics show that it occurred 
in 11 per cent of the latter as against only 5.5 per cent in the former; 
Sorgo found the ratio as 11 and 13.5 per cent respectively; while 
Berthold Miiller? found it in equal proportion in both sexes. 

Some nineteen hundred years ago Aretaeus described the ‘“ hemop- 
tysical constitution” as distinguished by brilliant whiteness of the skin, 
bright redness of the cheeks, narrowness of the chest, alar scapule, 
slenderness of the limbs and trunk, combined with a certain degree of 
adipose and lymphatic stoutness. Laennec said that phthisical subjects 
possessing this bodily configuration are more subject to hemoptysis 
than others. 

Patients with a nervous and excitable temperament are more apt 
to suffer from this complication than the indolent and phlegmatic. 
During some animated conversation, overexertion, singing, running, 
mountain climbing, straining at stool, or as a result of traumatism, 
hemorrhage may be provoked. But we should not overestimate over- 
exertion as a factor in the causation of hemoptysis. Streaky sputum, or 
mild hemorrhages may be caused by overwork or excitement. But 
copious hemorrhages are due to rupture of an aneurysm of Rasmussen, 
or the erosion of a comparatively large branch of the pulmonary artery 
by a tubercle. Perhaps the fact that the majority of copious and fatal 
hemorrhages occur during the night shows clearly that overexertion 


1 Ztschr. f. Tuberk., 1908, 12, 209. 
2 Causes and Results of Pulmonary Hemorrhages, London, 1879. 
3 Ztschr. f. Tuberk., 1910, 13, 133. 


16 


242 HEMOPTYSIS 


isnot the main factor. We are in the dark as to why these hemorrhages 
are more likely to occur during the night. Consumptives who have 
been urged on to eat excessively, becoming plethoric, ruddy, and fat, 
bleed more often than those who eat well, but moderately. Exposure 
to the inclemencies of the weather may excite hemoptysis, probably by 
causing an acute localized congestive and pneumonic process at the site 
of the tuberculous lesion. Coitus may excite it, and I have known two 
cases of fatal hemorrhage which occurred soon after intercourse. 

Certain drugs used extensively in phthisiotherapy, as arsenic, 
cresote and its derivatives, the iodides, aspirin, etc., are often instru- 
mental in bringing on hemoptysis. It has been stated that residence 
in high altitudes favors hemoptysis, but it has not been proved; as 
will be shown elsewhere, the prognosis of hemorrhage appears to be 
worse in these regions than at sea level. 

Some authors have found that there are seasonal influences in the 
production of hemoptysis, saying that the spring and summer months 
give the highest incidence, while Anders’s collective investigations show 
that it is most prevalent in the months of December, January, and 
February; August, September, May, and March, in the order named, 
seemed to rank next. The experience at the Phipps Institute coincides 
with that of Anders. Burns! says that “barometer changes seem 
to have little effect on the symptomatology. In a few instances hemor- 
rhages have occurred following a fall in the barometer, but in insufficient 
number of cases to justify constant relation. It is probably a matter 
of coincidence only so far as the barometer alone is concerned. There 
is a larger number of patients streaking in March, May and especially 
June than in other months. Hemorrhage occurred more frequently 
in June than in any other month.” 

I have observed in my hospital work that hemorrhages at times occur 
in epidemic form, a large number of patients bleed at the same time 
in a ward. This may be explained by. some intercurrent infection, 
especially influenza, causing pulmonary congestion. But psychic in- 
fluences may also be at work. 

Any of the above-mentioned factors may be the apparent exciting 
cause, but this is not true of the majority of cases. In my experience, 
a large proportion of hemorrhages, especially copious ones, begin when 
the patients have the least reason to expect them. It is the universal 
experience in sanatoriums that patients who have been kept under 
a rigorous rest cure may bleed. As was already mentioned, more than 
one-half the serious hemorrhages begin during the night, when the 
patient is resting in bed, or sleeping, and suddenly wakes up with 
cough, followed by a mouthful of blood. In patients with eroded . 
bloodvessels or miliary aneurysms in the lungs, bleeding is apt to occur 
without any known provocative cause, and usually it cannot be pre- 
vented by any known means. 


1 Boston Med. and Surg. Jour., 1914, 170, 564. 


STREAKY SPUTUM 243 


Diagnostic Significance of Hemoptysis.—It has been repeatedly 
stated that all patients with hemoptysis should be considered tubercu- 
lous and treated accordingly, until the bleeding is proved to be due to 
some other cause. But just because the vast majority of hemoptyses 
are due to tuberculosis of the lungs, when the blood is derived from 
some other source, it at times proves a serious source of error. There 
is left a wide margin of error when we attempt to follow this principle 
of considering every case of hemoptysis as tuberculous. Cabot among 
3444 cases of hemoptysis treated at the Massachusetts General Hos- 
pital, found only in 1723, or 50 per cent, was the bleeding due to 
phthisis; Jex-Blake, in 54.6 per cent of 909 patients; and Stricker 
77.6 per cent of 900 patients with a history of hemoptysis. Ware, 
among his private patients, observed 386 cases of hemoptysis among 
whom no less than 62 showed no evidence of disease, which would 
explain the occurrence of blood-spitting. Among the patients who 
consult me at my office, fully 50 per cent of those who have hemoptysis 
are not at all phthisical. 

The most perplexing cases that present themselves in physicians’ 
offices are patients who claim that several days ago they expectorated 
blood. In many the blood was derived from the nose, throat, gums, 
etc. Examination of these parts may not reveal any irritation, hypere- 
mia or varices, while in the chest there are found some indefinite signs 
of an apical lesion which may be of non-tuberculous origin, or some 
changes in resonance and breath sounds indicating a perfectly healed 
lesion, thus leading to an erroneous diagnosis of active tuberculosis. 
This is especially seen in cases of epistaxis in which the blood trickled 
down the posterior nares, exciting cough productive of blood, or blood- 
streaked sputum. Some patients have epistaxis during the night, 
wake up spitting blood and present themselves promptly in the morn- 
ing for a medical examination which does not reveal any definite clues 
as to the source of the bleeding. 

Streaky Sputum.—Great care must be exercised before diagnosing 
tuberculosis based on a history of blood-streaked sputum. While 
this, when originating in the lungs, may, in rare cases, be a precursor 
of a large and profuse hemorrhage, it is, however, a fact that streaky 
sputum only rarely originates in the pulmonary parenchyma; in the vast 
majority it comes from the nose, throat and especially the bronchi. 
West! says that streaky hemoptysis is far more frequent in bronchitis 
than in phthisis. When it occurs in phthisis it is generally due to the 
same cause, viz., the rupture of distended capillaries in the bronchial 
tubes as the result of violent coughing; but when the tubes are the seat 
of tuberculous ulceration, bleeding may sometimes take place from the 
ulcerated surface, usually in small amount and streaky, but occasion- 
ally in larger amount. Individuals suffering from chronic rhino- 
pharyngeal and subacute tonsillar inflammation of any sort at times 


1 Diseases of the Organs of Respiration, London, 1909, 2, 381. 


244 HEMOPTYSIS 


expectorate blood-streaked sputum. This occurs largely in the morn- 
ing; while “clearing the throat” some mucus is expectorated showing 
streaks of blood. The patient is frightened, and with a view of con- 
vincing himself, begins to cough more strongly, finding on inspecting 
the material that it really does contain blood. The force used to dis- 
lodge the attached secretions may be responsible for the streaks of 
blood brought out. A careful examination of the throat may not show 
anything suggestive of the source of the blood. 

In addition to rhinopharyngeal inflammatory processes there are 
other conditions of the throat which may produce hemoptysis. Among 
them may be mentioned certain new growths of the larynx, such as 
vascular fibromas, hemorrhagic laryngitis, etc. In several cases under 
my care these non-tuberculous conditions proved to be a source of error. 

In many cases with a history of streaky sputum a diagnosis can 
only be arrived at by careful observation of the patient for weeks, after 
the presence or absence of fever, tachycardia, anorexia and physical 
signs in the chest are diligently studied. Very often the blood is 
derived from congestion in chronic pharyngitis with a spongy mucous 
membrane, or from dilated or varicose bloodvessels in the trachea, or 
main bronchi, common in asthma and chronic bronchitis. Varicosities 
of the esophagus are also said to be quite common. These “esophageal 
piles’ may cause very copious hemorrhages. Many writers have 
described hemoptysis due to varices at the base of the tongue which are 
visible in the laryngeal mirror. The veins may be large and dilated and 
often extend to the fold of the epiglottis, or only a number of blue or 
dark blue specks may be noted, at times confluent, greatly resembling a 
vascular tumor. These are very often causes of hemoptysis. They 
are found mostly in persons between forty and fifty years of age, 
especially those who show stigmata of arteriosclerosis and other vari- 
cosities, as on the legs, or hemorrhoids. 

These false hemoptyses have been described by many English 
physicians. Williams! speaks of persons who, without any symptoms 
of lung disease, bring up quantities of blood and recover without 
permanent cough. He says that they were generally middle-aged and 
often had the arcus senilis. Recovery is the rule. Several cases of 
this class come within the writer’s observation annually. Sir Andrew 
Clark? also describes “arthritic hemoptysis” occurring in elderly per- 
sons free from ordinary disease of the heart and lungs; a form of hemop- 
tysis arising out of minute structural alterations in the terminal blood- 
vessels of the lung. These vascular changes occur in persons of the 
arthritic diathesis, resemble the vascular alterations found in osteo- 
arthritic articulations, and are themselves of an arthritic nature. More 
recently I. de Havilland Hall? attributed these hemorrhages to high 

rascular tension. [Even though it occurs in a patient who has had 


1 Pulmonary Consumption, London, 1887, p. 135. 
2 Tr. Med. Soc. of London, 1889, 12, 9; Lancet, 1889, 2, 840. 
3 Lancet, 1915, 2, 329. 


HEMOPTYSIS IN HEART DISEASE 245 


phthisis, this form of hemoptysis is not necessarily due to a recru- 
descence of the disease, but may be the result of high tension with 
degenerate vessels. 

At times persons suffering from pulmonary emphysema expectorate 
blood-streaked sputum, especially after paroxysmal cough. In rare 
instances I have observed emphysematous subjects expectorating pure 
blood—as much as an ounce or two. While in such cases we always 
suspect that we are dealing with the emphysematous form of fibroid 
phthisis (see p. 422), yet I have seen many cases in which subsequent 
observation, for a long period of time, has shown conclusively that 
no active tuberculosis developed. 

Hemoptysis during Acute Respiratory Diseases—We have already 
mentioned that acute rhinitis, pharyngitis, tonsillitis, etc., may be 
accompanied by the expectoration of blood. In fact, when a patient 
complains of hemoptysis and shows signs and symptoms of an acute 
affection of the upper respiratory tract the chances are greatly in favor 
of the blood being derived from the rhinopharynx and not from the 
lungs. Moreover, tuberculosis never begins with acute coryza, pharyn- 
gitis, or tonsillitis. 

In lobar pneumonia the rusty sputum is characteristic. But in many 
cases the expectoration of pure, bright red blood is observed. In bron- 
chopneumonia, hemoptysis is even more frequent, and during the recent 
epidemic of influenza a large proportion of patients in whom pneumonia 
complicated the process had more or less profuse hemorrhages. ‘The 
differentiation is made by the history of the case, its epidemic occur- 
rence, the symptomatology which is characteristic of influenza, and 
the location of the pulmonary lesions. 

Hemoptysis in Pleurisy.—In many cases of pleurisy with effusion the 
onset is with a more or less copious pulmonary hemorrhage. I have met 
many cases in which after the bleeding ceased physical examination 
revealed an effusion into the pleura. In some phthisis developed sub- 
sequently, but others remained well for an indefinite time after the 
effusion was absorbed. I have also noted that this is more likely to 
occur in cases of interlobar pleurisy, first described by Dieulafoy. 
There may be blood-streaked sputum, and at times abundant hemop- 
tysis, which may recur at variable intervals. After the interlobar 
effusion has been absorbed, or an abscess remains after an interlobar 
empyema, recurrent attacks of hemoptysis may occur. ‘The differen- 
tiation of these cases from tuberculosis is discussed elsewhere in this 
book. 

Hemoptysis in Heart Disease.—Blood-spitting in heart disease is 
often treated as of tuberculous origin with disastrous results. Inas- 
much as we very often meet with cardiacs who are emaciated, cough, 
and have occasionally mild pyrexia, the diagnosis of tuberculosis is 
at times made erroneously. It is in fact usually supported by some 
physical signs in the chest, because cardiacs may show defective 
resonance, alteration in breath sounds, and even rales over an apex, 


246 HEMOPTYSIS 


or other parts of the chest as a result of infarction, peripheral throm- 
bosis, or brown induration. I have seen cases of organic heart disease 
treated in tuberculosis clinics and day camps in New York City for 
months. In infarction the expectorated blood may be bright red, 
and very copious in rare cases, but in mitral disease small, solid, purple 
or black lumps, which sink in water, are usually brought up. They are 
derived from ruptured capillaries in the walls of air cells, where they 
remain for some time before they are expectorated. The experienced 
eye can generally distinguish them. 

According to Frederick W. Price,! mitral stenosis is probably the 
next most frequent cause of hemoptysis to pulmonary tuberculosis, 
and a common source of error. Among 3444 cases of hemoptysis in 
the Massachusetts General Hospital, R. Cabot? found that in 1177, 
or over 34 per cent, the bleeding was due to mitral disease. Perhaps 
the heart is not examined at all, or if it be examined it is by no means 
rare for the characteristic murmur to be absent. Furthermore, because 
there are frequently apical signs, as has already been indicated, phthisis 
is often diagnosed. In several cases I was nearly trapped by this 
similarity of mitral disease to phthisis, but noting some irregularity in 
the heart-beat, I investigated further and diagnosed mitral stenosis. 
It must always be remembered that while active phthisis is not alto- 
gether excluded with heart disease, yet it is extremely rare, especially 
in mitral stenosis. 

In aneurysm of the aorta the end often comes through a rupture of the 
sac and fatal hemorrhage occurs. But in many cases streaky sputum 
is seen for weeks, or even for months, before the fatal hemorrhage 
finally kills. I have seen several cases in which pressure exerted by 
the aneurysm on the lung, or on a bronchus, produced signs simulating 
an apical lesion, and it is not exceedingly rare to find that cases 
admitted to and kept for months in sanatoriums are found suffering 
altogether from aneurysm of the aorta. 

In pulmonary infarction hemorrhage is the rule. Mistakes of con- 
founding these cases with tuberculosis may be avoided by a careful 
consideration of the history of the patient, an examination of the 
peripheral veins, the heart, etc. Still, many of these patients are often 
treated for tuberculosis because of the hemorrhage (see p. 552). 

Hemoptysis in Bronchiectasis, Syphilis, and Cancer of the Lungs.—In 
bronchiectasis bleeding is not uncommon, and I have seen copious 
hemorrhages due to this cause. The blood is derived either from dilated 
and congested bloodvessels in the proliferated mucous membrane, 
or from inflammatory changes in the mucosa, or from small eroded 
aneurysms in the walls of bronchiectatic cavities, similar to those 
found in tuberculous excavations. As a rule, it is encountered in older 
persons, but recently, since bronchiectasis has become quite common 
as a sequel of influenzal bronchopneumonia, we find hemoptysis due 


1 British Med. Jour., 1912, 1, 287. 
2 Differential Diagnosis, 1914, 2, 433. 


MENSTRUAL HEMOPTYSIS 947 


to this cause among younger persons very frequently. During the 
hemorrhage the diagnosis may be difficult, though a careful history 
clears up the case. In syphilis of the lungs, hemoptysis of various 
degrees has been encountered. 

Hemoptysis often occurs in cases of cancer of the lung, and is at times 
a source of error in diagnosis. In the early stages of cancer of the lung 
the symptoms may panies those of iheralccd very closely. The 
bleeding, if it does occur, is usually very obstinate; the patient keeps 
on expectorating dark clots of blood. Pure, bright blood is rare at 
this stage. The differential diagnosis is discussed in its proper place 
(see p. 547). In advanced cancer of the lung there may occur copious 
pulmonary hemorrhages. 

Other pulmonary diseases which may cause hemoptysis are fibrinous 
bronchitis, some cases of gangrene of the lung, echinococcus, pulmonary 
spirochetosis, and actinomycosis of the lungs. The differential diag- 
nosis 1s discussed in Chapter XXVIII. 

Hemorrhages from the Esophagus.—Varicosities of the esophagus, 
“esophageal piles,” have already been mentioned as liable to cause 
hemorrhages which closely simulate pulmonary hemoptysis. In one 
case under my observation the bleeding was copious, almost threaten- 
ing, and a diagnosis could not be made for some time. There have been 
reported cases in which the mucous membrane of the gullet was covered 
by enlarged, dilated, and tortuous veins. It is mostly found in persons 
suffering from cirrhosis of the liver. But it may occur in those who have 
no hepatic trouble. Patients suffering from cancer of the esophagus 
also may bring up blood with their expectoration ; in the advanced 
stages of the disease the bleeding may be copious. The neoplasm may 
extend to, and perforate a bronchus and the blood may thus be brought 
out through the trachea and larynx. The diagnosis should offer no 
difficulties to those who carefully examine their patients. 

Menstrual Hemoptysis.—Phthisical women, if they are to have 
hemoptysis at all, are more apt to have it during the menstrual period. 
It has been observed that during menstruation there is usually an 
increased blood-pressure and congestion of the laryngeal mucous 
membrane, and some state that active periodical hyperemia of the 
lungs occurs at that time and this would favor extravasation of blood, 
especially in the affected area. According to Macht! these periodical 
hemorrhages, which may be very slight or profuse, may persist after 
the patient has improved in health and the tuberculous process becomes 
arrested. Periodic hemorrhages in consumptives at the time of 
menstruation may take place from other organs than the lungs. Thus, 
Wilson and Newman have reported such hemorrhages from the trachea 
and upper respiratory passages. Macht also reports a rather inter- 
esting case of a woman with pulmonary tuberculosis with intestinal 
complications—uleer in the bowels—who regularly had severe hemor- 
rhages from her intestines at her periods. 


1 Am. Jour. Med. Sci., 1910, 140, 835. 


248 HEMOPTYSIS 


Vicarious menstruation, which is very rare, appears to be due in 
most cases to tuberculosis. But in evaluating vicarious menstruation 
it must be borne in mind that amenorrhea is very frequent in phthisis, 
and in this disease hemoptysis is frequent; it is therefore not surprising 
that hemoptysis should occasionally occur while the menstrual flow 
has been delayed or suppressed. 

Hemoptysis is apt to occur in pregnant tuberculous women periodi- 
cally almost to an extent as to suggest that it is vicarious in character. 
On the other hand, non-tuberculous pregnant women have hemoptysis 
at times, especially if they cough severely for any reason. Many cases 
of this sort have come under my observation. After childbirth they 
usually cease bleeding if they are not tuberculous. The diagnosis in 
these cases is very difficult at times because incipient phthisis often 
improves during pregnancy and is thus liable to lead to a false sense of 
security. A careful examination of the chest and several microscopic 
examinations of the sputum will, however, clear up the case in most 
instances. 

Several authors have also reported hemoptysis in women during 
lactation; soon after the infant is weaned, they stop expectorating 
blood. The causes of these hemoptyses are obscure. 

Hemoptysis of Nervous Origin.—In hysterical individuals, especially 
women, we at times observe symptoms of incipient phthisis, including 
hemoptysis, but repeated physical examinations do not disclose any 
pathological changes in the lungs. Physicians of former generations 
have therefore spoken of “hysterical hemoptysis.’ In most of these 
cases we find that the blood is derived from the gums, or from the 
throat, brought out by violent cough. In their efforts to excite sym- 
pathy they are even apt to produce bleeding mechanically by injuring 
the buccal mucous membrane. When with this there is also cough, 
dyspnea, pain in the chest, and even fever, symptoms commonly found 
in hysterical subjects looking for sympathy, the diagnosis is at times 
very difficult. However, in addition to the absence of signs of a lung 
lesion, there are found positive stigmata of hysteria. On the other 
hand, the fact must not be lost sight of that hysterical individuals may 
become tuberculous, and that tuberculous individuals are often mani- 
festing symptoms of hysteria. Indeed, some patients who have had 
one or more attacks of hemoptysis become obsessed with the fear for 
blood and consider themselves the most unfortunate among tuberculous 
patients. When told by the physician that their disease is progressing 
rather favorably, they often retort, “Why, doctor, | am a hemorrhage 
case.” This is mostly seen in patients who have spent some time in 
sanatoriums and have either bled themselves, or observed copious, 
perhaps fatal hemorrhages in other patients. They constantly watch 
their expectoration for blood and may, during a fit of cough during 
the night, rise, light up the room and carefully inspect the sputum 
brought out with a view of finding a speck of blood. This fear for bleed- 
ing, which one author has called hemophobia, may dominate the entire 


HEMOPTYSIS OF UNKNOWN ORIGIN 249 


clinical picture, and it is at times difficult to manage this class of 
patients. 

In certain diseases of the central, as well as the peripheral nervous 
system, hemoptysis may occur. Thus, in some cases of locomotor 
ataxia, cerebral hemorrhage, etc., hemoptysis is at times observed, 
though a careful examination of the chest fails to reveal signs of 
a pulmonary lesion. In some cases of epilepsy also it has been 
observed that the patients expectorate blood after a paroxysm. In 
these cases the blood may be derived from the tongue, which was 
injured by the teeth. It has, however, been shown that disturbances 
in the central nervous system may result in hemoptysis. Experiments 
by Brown-Séquard demonstrated that after injuries to the pons Varolii 
there were extravasations of blood into the lung tissue. Francois-Frank 
found that strong irritations of the peripheral nerves may result in 
bleeding from the lungs. Lichtheim, Claude Bernard, Longet, and 
other physiologists have confirmed these experimental findings. 

It must, however, not be rashly concluded that tabetics who expec- 
torate blood are not tuberculous. In most cases that came under my 
observation the tuberculous lesions were localized, or positive sputum 
was obtained. But it appears to the writer that the lung lesions are 
usually quiescent; active and progressive phthisis is rare in tabetics, 
perhaps because of the syphilitic substratum. In rare cases hemop- 
tysis in tabetics was found to be distinctly non-tuberculous in character. 

Hemoptysis of Unknown Origin—We have already mentioned that 
every physician of experience has met with cases of hemoptysis showing 
no symptoms or signs of any disease to account for the bleeding. Very 
frequently we are consulted by patients in whom the most painstaking 
examination and clinical observation extending over a long period of 
time reveal no cause for the pulmonary hemorrhage. They remain 
healthy indefinitely. In some the hemorrhages are recurring at irreg- 
ular intervals, and at times the amount of blood brought out may be 
considerable. The patient after losing considerable blood remains 
anemic for some time, but soon recuperates, and feels well indefinitely. 
Various suggestions may be made as to the origin of the bleeding, but 
none can be proved to the satisfaction of those who are competent to 
pass an opinion. Those who consider these pulmonary hemorrhages as 
of the same diagnostic significance as epistaxis are as safe in their 
assertions as those who are more explicit and careful in their diag- 
nostic utterances. 

I have met with several of this type of cases treated as tuberculous, 
kept in sanatoriums, or banished to distant climes. But they never 
developed symptoms of active pulmonary phthisis. Emanuel Libman 
and Reuben Ottenberg speak of hereditary hemoptysis. They have 
observed a case in which for four generations more or less copious 
hemorrhages from the lungs occurred at irregular intervals, and in no 
instance has phthisis developed. Similarly epistaxis is occasionally 
seen to run in families. With hemoptysis, however, there is always 


250 HEMOPTYSIS 


danger that the patient will be pronounced affected with hereditary 
tuberculosis and treated as such, though in fact it is of no more sig- 
nificance than a nose bleed. 

Some of these hemoptyses of unknown origin may be due to abortive 
tuberculosis (see p. 414). In others they are due to bronchiectasis which 
is not easily diagnosticated. In one case under my observation for 
eight years tuberculosis was diagnosticated and institutional treatment 
instituted; then other conditions were accused, but finally we made 
up our minds that it is due to multiple bronchiectatic cavities. The 
bleeding in this case occurs at irregular intervals, is nearly always 
copious and even threatening, the patient remaining exsanguinated, 
but soon recuperates. It seems that phlebotomy prevents the hemor- 
rhage in this patient, or at least mitigates its severity. 

Localization of the Source of the Hemorrhage.—Heretofore the deter- 
mination of the side of the chest in which the bleeding takes place 
was merely of academic interest, because it made very little difference 
on which side the ice-bag, which has been traditionally used in the 
treatment of this symptom, was applied. But recently, since we found 
that an artificial pneumothorax may stop a copious hemorrhage after 
everything else has failed, it is of practical importance to localize the 
bleeding-point. 

In cases which have been under observation for some time, and it 
is known that the lesion is unilateral, the problem may be simple, 
inasmuch as profuse bleeding usually implies a cavitary lesion. But in 
bilateral cases it is difficult, often impossible, to determine positively 
which lung is bleeding. Percussion must not be done for fear of in- 
creasing the bleeding, and auscultation may be of service in showing 
a limited area of moist, consonating rales, and perhaps amphoric 
breath sounds. But it is a noteworthy fact, which must never be lost 
sight of, that during profuse hemorrhages the blood may be aspirated 
into the non-bleeding lung and produce all sorts of rales. It is there- 
fore, at times, impossible to decide positively which lung is bleeding. 

In rare instances we hear murmurs, synchronous with the heart-beat, 
over the site of excavations. Gerhardt found that these murmurs 
originate in arteries which traverse the walls of cavities and he verified 
his observations at the autopsy table. In several cases this phenomenon 
was observed by me, the murmur was audible below the clavicle, and 
over the same area were most of the classical signs of pulmonary 
excavation. These patients are apt to bleed copiously, and they often 
succumb to a sharp hemorrhage. Here we know that the source of 
the bleeding is the branch of the pulmonary artery which traverses 
the cavity, and operative treatment (an artificial pneumothorax) may 
be attempted when a hemorrhage cannot be controlled otherwise. 
But these cases are rare and in the average case we cannot say with 
any degree of certainty that the bleeding vessel is located in a super- 
ficially recognized excavation, and not in another one, either located 
deeper, or altogether in the other half of the chest. I have repeatedly 


DIFFERENTIAL DIAGNOSIS 951 


seen cases in which after a copious hemorrhage the more affected side 
remained unaltered, while in the unaffected lung signs of a new lesion 
appeared. 

According to Stricker,! the bleeding comes from an eroded vessel 
when it occurs suddenly during the course of acute and progressive 
phthisis, while in chronic cavitary phthisis it is usually derived from 
an aneurysmal dilatation of a vessel. Repeated hemorrhages accom- 
panied by fever point to progressive decay of the affected area in the 
lung. -Hemoptysis in the advanced stages of phthisis is derived from 
eroded arteries, and for this reason the prognosis is less favorable 
than in hemoptysis in incipient cases or in initial hemorrhages, which 
are, as a rule, of venous origin. 

Differential Diagnosis.—In cases of initial hemoptysis it is impera- 
tive to ascertain whether the blood is derived from a tuberculous 
lesion or js due to some other cause. Jt must never be lost sight of that 
hemoptysis may be a symptom of every disease of the wpper and lower 
respiratory tracts, tuberculous as well as others. Careful examination of 
the nose and throat may reveal that it is altogether due to congestion or 
varicosity of the mucous membranes of the upper respiratory tract, as 
has already been mentioned. When the sanguineous fluid expectorated 
is uniformly bright red and watery, it is, in all probability, derived from 
the mouth. In case no symptoms or signs of a pulmonary lesion are 
discovered, and the bleeding cannot be ascribed to a non-tuberculous 
condition, the heart is normal, and there is no history of an injury, the 
patient is to be placed under prolonged observation before deciding 
that he is not tuberculous. But it must always be borne in mind that 
mere streaks in the sputum may be due to many causes other than tuber- 
culosis of the lungs, and a diagnosis of phthisis should not be made because 
of their presence alone. 

In copious hemorrhage, when it is not feasible to examine the 
patient’s chest carefully, it is often difficult to decide whether the 
bleeding is due to a tuberculous lesion, a bronchiectatic cavity, pul- 
monary syphilis or, in rare cases, whether it is not altogether hema- 
temesis. The last-mentioned condition may simulate hemoptysis 
because the patient may have aspirated the blood into the respiratory 
passages and then expectorated it; while in hemoptysis the blood may 
be swallowed and then vomited. It may then greatly simulate blood 
derived from the stomach, viz., black or chocolate-colored, thick 
lumps or clots, mixed with the contents of the stomach, and the stools 
may subsequently show evidences of blood. I have met with cases 
in which the diagnosis could not be made immediately, and I have 
seen several tuberculous patients in whom ulcer of the stomach was 
diagnosed and they were operated upon. We may, however, be guided 
by the following points: In hemoptysis the blood is, as a rule, coughed 
up, bright red, frothy and mixed with sputum. It is also alkaline and 


1 Nothnagel’s Handbuch d. spez. Pathol., 14, 7. 


252 HEMOPTYSIS 


does not clot. But many patients swallow the blood and then vomit 
it out; it is then acid in reaction. Auscultation may reveal rales in 
some part of the chest, and a careful history will show that the patient 
has been coughing, expectorating, etc., for a long time, while in cases 
of hematemesis the history points to disturbances in the gastric func- 
tions, and physical signs may be discovered in the abdomen. In hemop- 
tysis we invariably observe that after the cessation of active bleeding the 
patient keeps on coughing and expectorating clotted blood for several days, 
which is never observed in hematemesis. But when the hemorrhage from 
either source is brisk and copious, and there is no history, the points 
just enumerated are often of little or no value, because the blood is 
bright red, alkaline, and not mixed with either sputum or gastric con- 
tents. However, such profuse hemorrhages are, as a rule, seen in 
advanced consumptives in whom there are always to be noted the 
stigmata of tuberculosis. 

In cases in which the diagnosis has not been previously established, 
bleeding from the deeper respiratory passages may, in rare instances, 
be difficult of differentiation as to whether it is derived from a tuber- 
culous lesion or from a bronchiectatic cavity. I have been guided by the 
pulse and temperature of the patient—when these are normal, and the 
general condition of the patient is good, the chances are that there is 
a bronchiectatic cavity, especially in persons over forty-five years of 
age. When physical examination shows that the lesion is localized in 
a lower lobe, while the apices are free from pathological changes, the 
disease is almost invariably non-tuberculous bronchiectasis, pulmonary 
abscess, gangrene, etc. In older persons with arteriosclerosis the 
so-called “arthritic diathesis” is to be thought of. Usually a careful 
history clears up the diagnosis, while in rare borderline cases we should 
reserve our opinion until the hemorrhage ceases and a careful exami- 
nation of the patient is feasible. 

In addition to tuberculosis the following conditions are liable to 
cause pulmonary hemorrhage: Cardiac disease, aneurysm of the aorta, 
hemophilia, bronchiectasis, syphilis, abscess, and gangrene of the lung, 
certain acute specific fevers, pneumonia, epidemic influenza, suppu- 
rative processes in the mediastinum, foreign bodies in the bronchi, 
injuries to the chest, paroxysms of pertussis, echinococcus, cancer, 
actinomycosis, aspergillosis, hydatid, bronchopulmonary spirochetosis, 
distoma pulmonale westermanni, and pneumokoniosis. 

Prognostic Significance of Hemoptysis.—Patients, almost without 
exception, overestimate the significance of hemoptysis and are more 
terrified at the appearance of a speck of blood in their sputum. than 
by any other symptom or complication of phthisis, excepting perhaps 
pneumothorax. It is for this reason that initial hemoptysis has been 
described by some authors as a salutary phenomenon, because it draws 
the attention of the patient to the condition of his lungs which he may 
have otherwise neglected. In fact, I have known cases in which hemop- 
tysis was actually life-saving for just this reason in patients who had 


DEATHS DUE TO PULMONARY HEMORRHAGES 253 


coughed for months, and presented other symptoms of phthisis, all of 
which they considered a trifling affair, when, like the climax of a slowly 
developing drama, hemoptysis made its appearance, opening their eyes, 
or even those of their physicians, so that proper treatment was 
instituted. 

A hemorrhage may prove fatal immediately or within a few days 
of its appearance; or, if the patient survives it, it may have an influ- 
ence on the course of the disease. 

Prognosis in Initial Tuberculous Hemoptysis.—We have already 
mentioned that in many cases pulmonary hemorrhage, even when due 
to tuberculous lesions, is not necessarily followed by symptoms of 
phthisis. Every physician has among his clientele patients who 
coughed out more or less blood years ago but have never suffered from 
any obvious disease of the lungs. ‘Outspoken tuberculosis does not 
necessarily follow hemoptysis,” says Frederick T. Lord,! “which may 
occur in patients with apparent good health and sound lungs. In 1768, 
Goethe, at the age of nineteen years, and then a student at Leipzig, 
had an attack as follows: ‘One night I waked with a severe hemoptysis 
and had enough strength and presence of mind to wake my room-mate 
. . .. for several days I wavered between life and death.’ For some 
months he thought he had pulmonary tuberculosis and must die young. 
At the age of eighty-two years he had hemoptysis again and died at 
the age of eighty-three years. His long and active life may serve as 
a comforting example to those who need encouragement. At the age 
of twenty-three or twenty-four years, Rousseau expectorated blood 
and gave up his work as a teacher of singing. He died at the age of 
sixty-six.” A fatal issue in initial hemoptysis is extremely rare. I 
have never seen one. 

Proportions of Deaths Due to Pulmonary Hemorrhages.— When profuse, 
the patient may be exsanguinated and succumb to cerebral anemia, 
or the blood may overflow the bronchial tree and suffocate him, 
especially when it occurs suddenly while the patient is asleep. While 
this outcome is seen now and then, it is a very rare occurrence. Louis 
had but 3 fatal cases in 300 consumptives; Williams 4 out of 198 
fatal cases; Wilson Fox 4 out of 101; Moeller saw only 1 fatal hemop- 
tysis during fifteen years’ experience with consumptives; Wolff reports 
a lethal outcome 3 times among 1200 tuberculous patients (0.25 
per cent); Winsch 1 among 200 (0.5 per cent); Thue, 13 times among 
975 patients (1.6 per cent); Sorgo 14 deaths among 5800 consumptives 
(2.4 per cent) and among 2.16 per cent of his patients subject to hemop- 
tysis. McCarthy reports that at the Boston Consumption Hospital 
400 deaths occurred during a period of two years, only 7 of which were 
due to hemorrhage. Lord reports that death as an immediate result 
of bleeding occurred in only 1 of 76 patients with hemoptysis at the 
Channing Home, and 2 of 142 at the Massachusetts General Hosital. 


1 Diseases of the Bronchi, Lungs and Pleura, Philadelphia, 1915, p. 360. 


254 HEMOPTYSIS 


Death as a consequence of extension of pulmonary infection for which 
the hemorrhage was responsible, occurred in 1 case at the Channing 
Home, and 6 other cases at the Massachusetts General Hospital. 

Williams reports that in 1000 cases, including 63 fatal ones where 
the patients had hemoptyses of one ounce and upward on one or more 
occasions, the average duration was seven years and six months; an 
average differing only by a few months from that of the total deaths. 
In 200 living cases of similarly extensive hemoptysis, the average was 
eight years and three months—about the same as that of the living 
cases generally. “It is only in the far-advanced stages that it is likely 
to curtail the duration of the disease. In early cases hemoptysis is 
comparatively unimportant,” concludes Williams. When we say that 
hardly one out of a thousand deaths due to tuberculosis is caused directly 
by hemorrhage, we are as near the true figure as possible; hardly 2 per 
cent of tuberculous patients who bleed succumb to this accident. 

Influence of Hemoptysis on the Course of Phthisis—The influence of 
hemorrhage on the course of the disease is misunderstood by the 
average patient and often overestimated by the physician. It may be 
said that so long as it does not prove fatal immediately, and this is 
rare, as we have just shown, it has no effect on the patient nor on the 
disease. Many older writers have stated that it often has a rather 
salutary effect, and not altogether without reason, as is proved by the 
course of many cases subsequent to hemorrhages. Lebert, Flint, 
Wilson Fox, and others state that hemorrhages may produce a sense 
of relief, and cough and expectoration previously existing may tem- 
porarily disappear. Williams says: “To many patients its occurrence 
seems beneficial rather than otherwise, for the congestion is thus 
relieved and the system not materially weakened by the loss of blood.” 
I have seen many cases in whom the disease took a turn for the better, 
soon after a more or less profuse hemorrhage, and others in which the 
cough, anorexia, pains in the chest, etc., were ameliorated or disappeared 
after this accident. We know that slight abstraction of blood is often 
beneficial inasmuch as it stimulates the blood-forming organs to produce 
more blood cells. 

The fear, formerly entertained, that the blood, spreading all over 
the bronchial tree, is apt to inoculate new areas and produce new lesions 
in hitherto unaffected parts of the lung is now known to be without 
sound foundation, because reinfection is difficult or even impossible 
in the vast majority of cases. To be sure, we find that the bronchi 
contain blood while auscultating a patient during, or immediately 
after, a hemorrhage, but this is usually transitory, disappearing by 
absorption or expectoration within a few days after the bleeding 
ceases, and the original pulmonary lesion, if not progressive, remains 
the same as it was before, pursuing the same course as if no such 
accident had occurred. Cases in which after a hemorrhage a quiescent 
lesion begins to pursue an acute or subacute course and tuberculous 
bronchopneumonia is found at the autopsy are, in all probability, 


INFLUENCE OF HEMOPTYSIS ON COURSE OF PHTHISIS 255 


due to a sudden reduction in the powers of resistance, about the causes 
of which we know nothing at present. They do occur now and then, 
but when taken in connection with the large number of hemoptyses 
in which this sequel does not occur, they are comparatively rare. In 
fact, H. J. Corper! found experimentally that bleeding an animal for 
days before, and continued throughout the period of tuberculous 
infection has no appreciable effect upon the tuberculous process. 

The fear of bronchopneumonia as a sequel to pulmonary hemor- 
rhage, entertained by many physicians, is not founded on fact. In 
afebrile patients, soon after the hemorrhage ceases, the temperature 
may be elevated for a few days, but within a week or so, after the 
effused blood is absorbed, the temperature comes down to the level at 
which it was before this accident. Hemorrhages occurring in febrile 
patients, at times, have the effect that after the cessation of the bleed- 
ing the patient is afebrile, as I have seen in many cases. On the other 
hand, many patients running high fever, when attacked by copious 
hemorrhage, continue with pyrexia after the hemorrhage ceases, and 
finally succumb to the active tuberculous process, or, more commonly, 
to miliary tuberculosis. How rarely bronchopneumonia follows pul- 
monary hemorrhage can be seen from figures published by C. G. 
Reinhardt Goodwin: Among 1000 odd cases admitted to the sana- 
torium under his care in ten years, only 1 case of this kind has been 
recorded. 

More than sixteen hundred years ago Galen stated that the prognosis 
of pulmonary hemorrhage depends on the fever which is apt to accom- 
pany it—afebrile cases recover, while in febrile cases the prognosis 
is gloomy. More extended experience in recent years has confirmed 
the opinion of this ancient and empirical clinician. 

In hemoptysis the immediate, and especially the ultimate, prognosis 
depends less on the bleeding, its abundance or even repetition, than on the 
extent of the pulmonary lesion and the symptoms which accompany or 
dominate the clinical picture, the subsequent course of the original disease 
phthisis—and the complications which may arise. When we find during 
a hemorrhage that a patient has a good, full pulse, less than 100 in 
frequency, and no fever or dyspnea, the immediate prognosis is good. 
If there are several repetitions of the hemorrhage during the subse- 
quent few days, the prognosis is, as a rule, favorable so long as the pulse 
is good and there is no fever. Even fever is of no grave significance if it 
lasts but a couple of days. It is then due to absorption of the blood 
remaining in the bronchi. It is only when the fever is high and per- 
sistent for several days that it assumes serious import. 

In case the pulse becomes small, soft, compressible, and rapid, we 
may be sure that the bleeding continues even if we do not see it brought 
up in large quantities through the mouth, for we may have internal 
hemorrhage in phthisis, the blood being retained in a large cavity, 





1 Tr. Am. Tubercul. Assn., 1920, 16, 360. 
2 Practitioner, 1917, 99, 288. 


256 HEMOPTYSIS 


while the feeble patient is unable to force it out by cough. This is 
especially apt to occur after large doses of morphine have been adminis- 
ered, or in severely emaciated persons. 

In cases which had been active before the onset of the bleeding, 
having had fever, tachycardia, emaciation, etc., the prognosis after 
cessation of the bleeding is usually the same as it would have been had 
there been no such complication. The temperature usually drops 
during a brisk hemorrhage, but it rises again and the course of the 
diseases continues unabated. But if the temperature has been normal, 
or only slightly elevated, and the pulseislessthan 100, full and bounding, 
the patient has a good appetite, and sedative drugs are judiciously, 
if at all, administered, the immediate as well as the ultimate outlook 
is indeed good. 

In most cases the findings on physical exploration of the chest 
after moderate hemoptysis remain the same as they were before that 
event, although on auscultation we usually hear moist, consonating 
rales which may not have been there before the onset of bleeding. 
These rales may persist for several weeks. In some cases we find that 
the area of dulness over the upper lobe extends because of caseous or 
necrotic changes engendered during the hemorrhage. This dulness 
may disappear after the clots have been absorbed, or after the resolu- 
tion of the pneumonic areas. More frequently it is in time supplanted 
by tympany due to excavation. 


CHARTER, XOL 


SYMPTOMS CAUSED BY DISTURBANCES IN THE GASTRO- 
INTESTINAL TRACT—THE SKIN—THE JOINTS. 


GASTRO-INTESTINAL SYMPTOMS. 


Frequency.—Some authors have stated that phthisis develops mostly 
in individuals who have been naturally bad eaters; others have main- 
tained that those suffering from gastric derangement are most likely 
to fall prey to the disease, and Grancher says that “all consumptives 
have been, are, or will become dyspeptics.” In practice we meet 
with many patients who have been treated for gastritis for a long 
time until the true nature of their disturbance became evident. The 
diagnostic, and especially the prognostic, significance of anorexia or 
gastritis In a disease which depends in its origin and outlook on proper 
nutrition, cannot be overestimated. 

As far back as 1826 Wilson Philip! drew attention to the fact that 
many cases of phthisis are preceded for some time by severe indiges- 
tion. In his excellent monograph on the “Dyspepsia of Phthisis,”’ 
W. Soltau Fenwick? quotes Todd, Sir James Clark, Budd, Bennett, 
Ancell, and other writers of the first half of the nineteenth century, 
to the effect that dyspepsia is a very frequent forerunner of phthisis. 
In those days some authors spoke of “gastric phthisis,’ and “ pre- 
tuberculous dyspepsia” is even now mentioned by many writers. 
There is no doubt that incipient phthisis, as we know it at present, 
was In those days not recognized, and evidently this has been respon- 
sible for the notion that phthisis is often preceded by dyspepsia. 

Recent investigations, however, do not confirm that gastro-intes- 
tinal disturbances are per se predisposing factors in the evolution of 
phthisis, though Fenwick says that, for his own part, he is quite con- 
vinced that there does exist a variety of dyspepsia which is peculiarly 
apt to be followed by pulmonary tuberculosis. 

As an early symptom of phthisis, dyspepsia is quite frequent. Hutch- 
inson’ found it in 92 per cent of his cases, and in 55 per cent it was 
quite severe; Levison,* in 74.6 per cent; Mohler and Funk,°® in 64.6 
per cent of 1000 consecutive cases. Samuel Fenwick, Dobell, Pollock, 
and others have found it in nearly similar proportions. W. Soltau 


1 Treatise on Indigestion, London, 1826, p. 323. 
2 Dyspepsia of Phthisis, London, 1894. 

3 Medical Times, 1855, 1, 583. 

4 Ohio State Med. Jour., May, 1905, 1, 204. 

5 Am, Jour. Med. Sci., 1916, 152, 355. 


17 


258 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


Fenwick states that “dyspeptic phenomena of sufficient severity to 
attract the attention of the patient are encountered in about 70 per 
cent of all cases of early phthisis, but that the early development of 
the disorder in any individual case depends to a great extent upon 
the sex of the patient, the type of the tubercular disease, and the 
previous condition of the digestive organs.” He found that it is more 
apt to occur in females than in males, and, in general, in that variety 
of phthisis which commences insidiously and progresses slowly. 

More recent investigations have only partly confirmed the findings 
of the above-mentioned clinicians, and there are writers who con- 
sider anorexia, though not a result of gastritis, a constant symptom 
of incipient phthisis, like fever, cough, nightsweats, emaciation, etc. 
An analysis of 3007 cases in the Phipps Institute! show ed that 55.3 
per cent presented symptoms referable to the stomach. It appears, 
however, that these gastric disturbances were in no way due to changes 
in the stomach peculiar to tuberculosis itself, the changes being such 
as might occur in any chronic wasting disease. Janowski? reports that 
among 700 patients, 35 per cent suffered from gastric disturbances, 
which were more often encountered in women than in men. With this 
Kuthy is also in agreement. He found that in 37.3 per cent of his 
male patients there were gastric disturbances, as against 50.1 per 
cent in his female patients. In the first stage, 38 per cent; in the 
second stage, 46.4 per cent; and in the third stage, 57.2 per cent showed 
these symptoms. 

Symptomatology.— One of the characteristics of the anorexia of phthisis 
is that, unlike the appetite in other diseases, vt 1s independent of the fever, 
in many cases. Many patients with but slight fever have an almost 
complete antipathy for food, while others, who have moderate fever, 
preserve an excellent appetite. Laségue said, “All patients who eat 
and digest their food well, despite having fever, are consumptives.” 
In acute pneumonic phthisis, which is often difficult to differentiate 
from lobar or lobular pheumonia, I have placed great reliance on this 
symptom: In pneumonia the anorexia is invariably complete, while 
in acute phthisis the appetite may be retained more or less, and in 
spite of a temperature of 103° or 104° F. the patient is apt to ask for 
nourishment. 

In incipient phthisis the appetite is often very capricious. One 
day a certain food is preferred, while the next it is despised. Morbid 
cravings are not uncommon, especially in women. A large proportion 
of patients cannot tolerate certain kinds of food—some will not eat 
meat, others refuse milk, eggs, etc. It seems to me, however, that the 
repugnance for milk and eggs is often not the result of the tuberculous 
process, but is an acquired characteristic, due to the stuffing with these 
articles of food which is so commonly carried to an extreme degree. 
Following the usual advice, “plenty of milk and eggs,” is likely to 


1 Tr. Nat. Assn. Study and Prevent. Tuberc., 1910, 6, 193, 
2 Ztschr, f, Tuberk., 1907, 10, 493, 


GASTRO-INTESTINAL SYMPTOMS 209 


ruin an excellent appetite, if carried to extremes. Two or three quarts 
of milk, and a half or one dozen raw eggs daily, which tuberculous 
patients often consume, may result in a strong repugnance to these 
articles. 

An aversion to fats of any kind ws very frequently observed in phthisical 
patients. Hutchinson noted this fact over sixty years ago, and stated 
that 71 per cent of his phthisical patients disliked fats; 33 per cent 
could take them in but small quantities; while only 5 per cent liked 
them. Fenwick noted a marked aversion to fat in 64 per cent, and 
many of his patients developed this peculiar antipathy many months, 
or even years, before the onset of the pulmonary disease. He observed 
that among families which exhibit a marked predisposition to tuber- 
culosis, it is not uncommon to find that several members possess a 
strong aversion to all forms of fat, and are often unable to partake of 
even a small quantity of this material without suffering from acidity, 
nausea, or attacks of biliousness. Occasionally we meet with tuber- 
culous patients who dislike carbohydrate, especially saccharine, foods, 
the ingestion of which causes more or less severe gastric discomfort. 

In many cases the anorexia improves with the improvement in the 
local condition in the lung; but we also meet with cases in which the 
tuberculous lesion is slowly progressing or quiescent, but the appetite 
improves, as if the organism had adapted itself to the tuberculous 
toxemia. In fact, almost insatiable hunger may be seen in rare 
instances. 

In the early stages of phthisis digestion is fair, or good, in most cases. 
Indeed, it appears to me that digestion in phthisis usually depends on 
the condition of the gastro-intestinal tract before the onset of the lung 
disease. As was already intimated, the excessive quantities of milk 
and raw eggs may be responsible for the symptoms of dyspepsia in 
many cases, such as pyrosis, belching, flatulence, bad taste in the 
mouth, etc. The fact that these symptoms may be relieved by appro- 
priate corrections in the diet is in favor of our contention. Excepting 
in advanced cases, and in alcoholics, vomiting, if it occurs at this stage, 
is due to cough, as has already been detailed when speaking of the 
emetic cough. In the advanced cases it is likely to be preceded by 
nausea, which is not the fact with the emetic cough. In many early 
cases symptoms of vagotonia are quite prominent and they may 
dominate the clinical picture. There may be heartburn, pain after 
meals, pyrosis, belching, salivation, hunger pain, etc. Yet an examina- 
tion of the stomach and its functions may not reveal anything to 
account for these symptoms. 

Causes of Anorexia.—It appears that the anorexia of phthisis is of 
toxic origin. Analyses of the gastric contents have not revealed any 
constant changes in the anatomy or functional activity of the stomach 
in the early stages of phthisis. In some cases hyperchlorhydria is 
found, in others hypochlorhydria, while in many others the free and 
combined acids remain in about normal proportions, Nor have any 


260 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


constant secretory or motor disturbances been observed. The physi- 
ology and pathology of the stomach in early phthisis, as studied by 
Klemperer, Hayem, Einhorn, Brieger, Fenwick, and others, show no 
characteristic functional changes. 

Many French authors, notably Marfan,! are of the opinion that 
the gastric symptoms in early phthisis are due to the general anemia 
wnich causes sluggish secretion of gastric juice, weakness of the smooth 
musculature, and hyperesthesia of the gastric nerve endings of the 
vagus. Fenwick, finding that the dyspepsia in phthisis is not a direct 
result of pyrexia, nor of direct irritation of the mucous membrane, 
concludes that it is probably due to the chronic absorption of certain 
toxic substances which are manufactured in the pulmonary cavities; 
but he describes a form of dyspepsia which often precedes the develop- 
ment of pulmonary tuberculosis, when cavities are out of the question. 

The gastric symptoms appear to be analogous with those observed 
in chlorosis, and the severe anemias, which cause ischemia of the diges- 
tive tract. But, as Janowski points out, many tuberculous patients 
without any anemia also suffer from gastric symptoms, and he con- 
cludes therefore that the anorexia is not invariably due to general 
anemia, but to ischemia of the gastric and intestinal mucosa. ‘This 
explains why so many different results have been obtained from 
analyses of the gastric contents. It is the paroxysmal proclivity of 
the gastric disturbances which is characteristic of early phthisis. It 
is also a fact that reported investigations of gastric functions do not 
discriminate, as a rule, between early and advanced, febrile and 
afebrile, acute and chronic, active and quiescent lesions. Hence the 
great differences in their findings. 

Gastric Symptoms in Advanced Phthisis—The anorexia and other 
gastric symptoms of early phthisis usually subside in cases pursuing . 
a favorable course and the patients recover. But in cases with pro- 
gressive disease, especially those characterized by pulmonary excava- 
tions, more or less severe symptoms of dyspepsia are present. Nearly 
a century ago Louis found that about two-thirds of his phthisical 
patients had shown signs of dilatation of the stomach. W. Soltau 
Fenwick found among 100 autopsies in cases of tuberculosis in which 
he took special notes on this point, that the lower margin of the viscus 
extended below the level of the navel in 64, and he says that it is rare 
while performing an autopsy on a phthisical subject to fail to encounter 
some increase in the dimensions of this viscus. The degree of gas- 
trectasis appears to bear a direct relation to the extent and chronicity 
of the pulmonary lesion. Of course, this gastrectasis may be pre- 
tuberculous—we have already shown that those with the asthenic 
constitution are more likely to contract phthisis than others. But it 
may also be one of the results of tuberculous toxemia which is effective 
in producing atony of muscles—both striated and smooth. 


1 Troubles et lesions gastriques dans la phtisie pulmonaire, Paris, 1887, 


GASTRO-INTESTINAL SYMPTOMS 261 


Chronic catarrh is very frequent, but true tuberculous ulcers are 
exceedingly rare, probably because the stomach contains comparatively 
little lymphoid tissue, and bacilli cannot reach there through this channel, 
and the acid secretions are inimical to the growth of tubercle bacilli. 
Fenwick, after a careful search, was able to discover the records of 24 
cases of this affection, several of which are, however, open to suspicion; 
while among the notes of 2000 necropsies on cases of phthisis performed 
at the Brompton Hospital he could find only 2 instances in which 
tuberculous ulcers of the stomach were discovered. Lauritz found 
4 cases of undoubted tuberculous ulcers in the stomach among 580; 
Melchior 6 in 848 autopsies, and Gassmann 6.13 per cent in 600 
autopsies. Mohler and Funk did not find a single instance of gastric 
ulcer in 85 autopsies, and in 128 consecutive autopsies made at the 
Montefiore Hospital on cases under the writer’s care only one case of 
tuberculous ulceration of the stomach was discovered. There have 
been reported cases of perforation of tuberculous gastric ulcers into 
the peritoneum, though this is exceedingly rare because of the inflam- 
matory adhesions which usually form around the ulcers and the peri- 
toneum. Simple gastric ulcers are not infrequently found at autopsies 
on tuberculous bodies, but the proportion is not higher than among 
patients who succumbed to any cause. 

In the vast majority of cases of advanced phthisis the appetite is 
poor; those who do attempt to eat usually display various distastes 
for certain foods, and even this is not constant—the appetite is often 
very capricious, and many develop morbid cravings. This is one 
of the reasons for difficulties in feeding phthisical patients in sana- 
toriums and hospitals. At times we meet with patients who retain an 
excellent appetite to the end and instances of bulimia are not unknown. 
Pain after eating, pyrosis, belching, etc., are very common, and vomit- 
ing is, at times, a prominent symptom. But while the emetic cough 
may be encountered in advanced cases, the vomiting at this stage is 
usually not of this type. They simply vomit because of gastritis, or 
dilatation of the stomach. This type of vomiting is usually preceded 
by nausea, belching, etc., and not by cough as in those having the 
emetic cough. Nausea and retching may persist for several hours after 
the vomiting, and the ejecta consist of sour food mixed with mucus. 
I have met with cases in which no food could be retained owing to 
vomiting, and some even with hematemesis. The prognosis in these 
cases is gloomy indeed. 

In hectic cases the gastritis is often very troublesome and, com- 
bined with vomiting, nightsweats, cough, diarrhea, etc., it is one of the 
terminal symptoms of phthisis. In many cases, however, the pul- 
monary symptoms overshadow the gastric phenomena, but very often 
the latter are sufficiently pronounced to require great care and atten- 
tion. The amyloid liver often contributes considerably to the digestive 
disturbances, and lardaceous changes in the bloodvessels of the stomach 
are not unknown. I have met with cases of this type, extremely 


262 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


emaciated, hardly able to move a limb, yet they asked for food which, 
when given by the nurse, was relished with an apparently voracious 
appetite. 

It appears that the dyspepsia of advanced phthisis is usually asso- 
ciated with pulmonary excavation, and is mainly caused by the pro- 
longed intoxication characteristic of progressive and advanced disease. 
A fruitful source of gastric derangement is swallowed sputum, more 
common in women. The sputum not only irritates the mucous mem- 
brane of the gastro-intestinal tract, but some of it is also absorbed and 
produces toxemia. ‘The mucous membrane of the gastro-intestinal tract 
eliminates poisons from the blood, which in their turn irritate these 
membranes, as is the case in acute mercurial poisoning in which mer- 
curial albuminates circulating in the blood are eliminated into the 
intestines where they cause severe diarrhea. The injection of large 
doses of tuberculin may also cause diarrhea. 

Intestinal Symptoms.—During the incipient stage of phthisis the 
bowels are unaffected in most cases, though we meet with constipation 
in a considerable proportion. But I doubt whether the proportion is 
higher than among people with modern habits of life, and dietetic 
conditions. In some cases the constipation is due to the sedative 
medication used for the control of the cough. 

Diarrhea may be one of the symptoms of incipient tuberculosis. 
It is met with mainly in patients at the two extremes of life—in chil- 
dren under ten years of age and in senile patients. In children the 
diarrhea may be the only symptom, while examination of the chest 
may show nothing conclusive, or signs of tracheobronchial adenopathy 
may be found. In aged patients who have felt quite well, even claim- 
ing that they have not coughed, a chronic and persistent diarrhea 
should be considered a sign that a careful examination of the chest is 
urgent. It will be found that there are signs of old phthisical lesions 
in the lungs, and the sputum may contain numerous tubercle bacilli. 
Very rarely diarrhea is one of the symptoms of incipient phthisis in 
young adults. 

In some patients the functions of the bowels remain more or less 
normal through the course of the disease, but this is rare. In most 
cases diarrhea makes its appearance with the advance of the disease. 
While in many cases it is due to tuberculous ulceration of the bowels, 
there are others in which it is caused by intestinal catarrh, very fre- 
quently the result of dietetic errors. In many the ingestion of large 
quantities of milk is responsible and eliminating milk from the diet 
promptly gives relief. In others the excessive amount of fat, mainly 
eggs, is responsible. Elsewhere it is pointed out that raw eggs are 
very frequently the cause of diarrhea (see Chapter XLI). Persons 
who have had intestinal trouble before the onset of phthisis are more 
liable to suffer from catarrhal diarrhea than others. As will be pointed 
out later when speaking of tuberculous ulceration of the intestine, the 


EMACIATION 263 


differential diagnosis is exceedingly difficult. The prognosis depends 
on the causation of the diarrhea. When due to amyloid degeneration 
or tuberculous ulceration of the intestines the prognosis is grave. 


EMACIATION. 


Emaciation is a cardinal symptom of phthisis; one of the triad 
mentioned by Richard Morton, the others being cough and fever. 
Popular lore, as well as medical experience, have always associated 
tuberculosis with emaciation. Phthisis (Greek, ¢4eocc), consumption, 
has its equivalent in every European language. That it is mainly 
due to the tuberculous toxemia, engendered by the metabolism of the 
tubercle bacilli, is evident from the fact that experimental tuberculosis 
is always accompanied by emaciation of the animals. 

In acute galloping consumption, and in miliary tuberculosis, the 
emaciation is progressive and frightful, much more rapid than in other 
febrile diseases, as pneumonia, typhoid, etc., and this is one of the most 
important points in the differentiation of acute tuberculosis from other 
acute diseases. In children, when during or after an attack of measles, 
pertussis, etc., the wasting becomes very marked and there is dyspnea, 
rapid pulse, etc., acute tuberculosis is to be suspected. 

While the malnutrition and wasting in phthisis are often caused, and 
always enhanced to a certain extent, by the gastro-intestinal disturb- 
ances which are concomitants of the disease in all its stages, we meet 
with emaciation almost constantly in active disease with fair gastro- 
intestinal functions. Some authors are inclined to attribute the ema- 
ciation to the lowered powers of absorption caused by a congenital 
narrowing of the lymph channels in the intestinal tract which is said 
to predispose to phthisis. But this has not been proved. 

Extent of Emaciation.—Not only does the subcutaneous adipose 
tissue waste, but the nitrogen-containing muscles also vanish with aston- 
ishing rapidity. It is noteworthy that the first muscles to waste are 
those of the thorax—the pectorales, the scapular, the intercostals, etc. 
In many incipient cases we see a striking contrast between the wasted 
and flabby muscles of the chest—and in women occasionally the wasted 
breasts—and the fairly preserved contour of the muscles on the 
extremities. Moreover, the muscles and subcutaneous tissue of the 
affected side of the chest waste earlier than those on the opposite and 
unaffected side. The result is that the supraclavicular and supra- 
spinous fossee are more or less deeply excavated. This characteristic 
of the muscular wasting has recently been made available for diagnosis 
by the excellent studies of Pottenger. In some early cases the face 
remains full and is thus apt to deceive as to the state of nutrition of 
the patient whose trunk and abdomen are markedly emaciated. 

Effects of Emaciation.—’The weakness, weariness, loss of strength 
and vigor of the consumptive are greatly due to the muscular atrophy 
even in the early stages of the disease, and one of the best signs of 


264 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


improvement is the regression in the muscular atrophy. There appears 
to be a direct relation between emaciation and the course of the 
disease. With each extension of the process in the lung, with each 
hemorrhage, there is a loss in weight, and with each improvement 
there is a gain in this direction, while in quiescent cases the weight 
remains unaltered. It may be stated that, with some exceptions to 
be mentioned later, the scale readings may be taken as a fair index of 
the evolution of phthisis, and when we consider it in connection with 
the temperature curve, we can follow the case, and interpret it from 
the prognostic standpoint, with a fair degree of safety. 

There are, however, exceptions: Patients in whom the disease has 
been arrested, 2. e., in whom a quiescent lesion is smouldering, are apt 
to remain underweight indefinitely, though they feel quite well, and 
are more or less efficient. 

When patients are progressively losing it is not advisable to tell 
them the extent of their malnutrition. The discouragement often pulls 
them down much further. Conversely, it is often observed that 
patients gain weight after changing their physician, entering a new 
sanatorium, etc., and thus gain a false impression that they are on 
the road to recovery. But after the novelty of the new surroundings 
has worn off, the gain ceases. They may then even lose progressively, 
and finally weigh less than before admission to the institution. To be 
of favorable prognostic significance, gain in weight must be persistent 
for several months. 

In some cases of phthisis the emaciation is rapid and extreme; 
within a few months the body of the victim is reduced to a skeleton. 
These are the cases in which the disease runs an acute and progressive 
course—galloping consumption. Now and then we meet with patients 
in whom the disease is chronic, lasting for many years, still the emacia- 
tion is severe; the ribs, robbed of their adipose covering, protrude 
between the atrophied intercostal muscles so that we are unable to 
adapt the bell of the stethoscope to the chest. This cachectic form of 
phthisis is mostly seen in old people, and, inasmuch as they have no 
fever and hardly cough, latent cancer is at times erroneously diagnos- 
ticated. 

Prognostic Significance of Emaciation.—Sanatoriums advertising 
their advantages usually show the average number of pounds gained by 
the patients during a certain period, and patients usually gauge their 
progress by the scale. This is correct in the vast majority of cases. 
An improving patient is one who gains in weight, and one who loses 
progressively is doomed. But to this there are exceptions. Gains in 
institutions, while the patient is under a rigorous rest cure and overfed 
for long periods, are good as far as they go. But in order that the 
patient should be pronounced improved, or cured, it is necessary that 
he should hold his gain after he becomes active at his occupation or 
at some other vocation which suits him. In this regard, the graduated 
labor system of Paterson at Fromley is superior to other forms Of 


EMACIATION 265 


institutional treatment. The gains attained at Fromley are said to be 
more lasting than those in the institutions where the inmates lead a 
lazy or indolent life. Similarly, patients who are treated at home, and 
allowed to do some work while under treatment, are more likely to keep 
their gains than the former class. 

We must be careful in evaluating gains in weight. Sometimes the 
patient keeps on gaining moderately while the disease is progressing 
and we wonder why this is so. A careful investigation may show that 
the lower limbs are edematous, and it is not fat and flesh which is 
responsible for the increase in weight, but dropsical fluid. 

At times we meet with patients in whom the lesion in the lungs is 
improving or stationary, and they have a good, or even a voracious, 
appetite, yet they keep on losing in weight. This is usually due to 
intestinal tuberculosis in which there may not be the characteristic 
diarrhea. This is a diagnostic point worth remembering, because it 
is often very difficult to decide whether the intestine is implicated in 
the process, and the prognosis depends so much on the condition of 
the bowels. 

Seasonal Influences.—The seasonal influences on the weight of con- 
sumptives are best studied in sanatoriums. It appears that there are 
significant differences in this regard. At North Reading, Mass., Burns! 
found that the minimum amount of weight loss occurs in the colder 
months; the maximum loss oecurs in the warmer months; and rapid 
increase in amount of emaciation appears during the spring months. 
Going hand-in-hand with this is the fact that deaths in July outnumber 
other months. At the Adirondack Cottage Sanitarium, Brown? 
found that the weight curve in pulmonary tuberculosis, if not influenced 
by change in climate or some other factors, rises from August to 
Christmas (sometimes to November), remains more or less stationary 
with minor fluctuations from Christmas to Easter (March), and sinks 
gradually from Easter to August. Brown adds that this corresponds 
closely to the normal weight curve. In Pennsylvania, Karl Schaffle 
finds the gains most marked during the fall and winter months. Among 
private patients in New York City I find that the summer months are 
not conducive to gains in weight, nor are the autumn months with their 
variable weather; but during the winter, especially during very cold 
seasons, the gains are extraordinary; even patients who are running 
low for one reason or another often gain somewhat, or remain 
stationary, during December, January, and February. 

This is not true of other climatic regions. In a careful study of the 
weights of consumptives in eight sanatoriums in Denmark, N. 5., 
Strandgaard* found that weekly weighing shows low gains during the 
winter and spring months from December to May. Then there is a 
distinct rise during the summer months, June, July, and August, reach- 

1 Boston Med. and Surg. Jour., 1914, 170, 564. 


2 Osler’s Modern Medicine, 1, 380. 
3 Beitr. z. klin. d. Tuberk., 1914, 32, 179. 


266 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


ing its maximum in September, and declining in October, and more 
so in November and reaching its minimum in December. This is the 
exact opposite of conditions in the United States. 

The subject deserves careful study in connection with meteorological 
conditions. 

Fat Consumption.—The term “fat consumption” may appear incon- 
gruous, but we meet with cases of active phthisis in which the pan- 
niculus adiposus is well preserved, or even with excessive obesity, the 
phthisiques gras of some French writers. I see several cases of this 
sort annually in my private and hospital work. They appear healthy, 
with florid cheeks and well-formed bodies, and their only trouble is 
that nobody believes they are tuberculous. They cough and expec- 
torate, often profusely, quantities of sputum with numerous tubercle 
bacilli, run a mild subfebrile temperature, at times have nightsweats. 
Many have more or less profuse hemoptysis and in two that were 
under my care the cause of death was copious terminal hemorrhage. 

When these patients present themselves for examination one is 
loath to make a diagnosis of phthisis even when physical exploration 
of the chest reveals a typical lesion in one or both lungs, or cavitation; 
which is not uncommon. The course of the disease is rather slow; 
we may follow them for years without noting any marked changes in 
their general condition despite the fact that the lesion in the lungs is 
progressing and excavations are forming. Of course, only positive 
sputum findings are convincing to some patients or even physicians. 

The obesity is mostly seen in female consumptives during or soon 
after the menopause, though I have met it in males, especially alco- 
holics and those having a history of syphilis. They usually have a 
voracious appetite and when told that they must eat well, they follow 
directions, often overdoing it. Combined with the rest which is urged 
and implicitly obeyed, the overfeeding is effective in producing fat, 
despite the activity of the disease. In tuberculosis implanted on pul- 
monary emphysema, and also in fibroid phthisis, the weight of the 
patients is often above the average, though real obesity is observed 
only rarely. 

Fat consumption is also observed in children, especially infants of 
tuberculous stock. They appear well nourished and fat, but when 
we examine their muscles we find them flaccid and soft. These “pasty” 
infants have no resistance against infection, and are carried off by any 
acute disease which flares up the dormant tuberculous lesions. Simi- 
larly, tuberculous meningitis and bronchopneumonia are often seen 
in rather fat children. 


THE SKIN. 


In addition to the wasting of the muscles and subcutaneous fat, 
atrophy of the skin is one of the early changes in phthisis, first 
described by Clarence L. Wheaton,! of Chicago, and then by Pottenger. 


1 Jour. Am. Med. Assn., 1910, 54, 2123. 


THE SKIN 267 


On inspection it is noted that the skin over the site of the lesion is 
thin and the subcutaneous tissue vanished. According to Pottenger, 
this is part and parcel of the general degeneration, and occurs after 
the process has existed for some time. It denotes chronicity rather 
than earliness, although it is often found over comparatively early 
tuberculous processes. In such cases it may be presumed that there 
was an old quiescent lesion which has become the seat of renewed 
activity. 

The complexion of the consumptive is usually pale, though at times 
we meet with patients advanced in the disease who have retained a 
florid color. In some the hectic flush is evident at first sight; it is 
mostly seen at the time when the daily rise in temperature occurs. 
Occasionally this redness appears only on one cheek, corresponding 
usually to the affected side of the lung, as is discussed elsewhere. In 





Fic. 45.—Tuberculides. (Ormsby.) 


fibroid phthisis, and in those with emphysema, in the advanced stages 
of which dilatation of the right heart occurs at times, there may be 
cyanosis of variable degree. Cyanosis is also a cardinal symptom of 
miliary tuberculosis. In many cases with extensive excavations in 
both lungs there is hardly any cyanosis, at most some livid tint of the 
lips may be elicited on careful observation, but in fibroid phthisis 
cyanosis is frequently marked. In far-advanced disease with amyloid 
changes, the skin shows the characteristic appearance of this condition. 
According to Meyer Solis-Cohen! between 25 and 33 per cent of tuber- 
culous patients exhibit flushing, burning, sweating, urticaria; between 
14 and 25 per cent subjective sensations of heat, angioneurotic edema, 
dermographia, etc., all of which he attributes to autonomic disturb- 
ance. 


1 Am. Revue Tuberc., 1917, 1, 289. 


268 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


Chloasma Phthisicorum.—Smooth, shining, and non-desquamating, 
yellowish-brown spots are occasionally seen quite early in the disease 
on the forehead and upper parts of the face. They are frequently 
single, but often confluent, forming large patches which in female 
patients may be a great source of annoyance. My experience with 
consumptives confirms the observation made long ago by Jeannin to 
the effect that chloasma phthisicorum is mostly seen in connection 
with enlarged glands, and that these patients only rarely suffer from 
hemoptysis. In fact, I have looked in all cases of hemorrhage that 
have come under my observation during the past five years and found 





Fie. 46.—Acnitis. Dr. Quinn’s case. (Ormsby.) 


no one with this eruption of the skin, while among my other patients 
it is quite frequent, especially among young chlorotic women. In 
them the physical signs of phthisis are indefinite, but amenorrhea is 
frequent. In advanced cases we often meet with brownish coloration 
of the skin, mostly marked on the face, but at times all over the body, 
simulating the smoky gray or bronze color seen in Addison’s disease. 
Considering the frequency with which the adrenals are found affected 
in consumptives, we have an explanation for this phenomenon. 

Patients who sweat profusely may show miliaria, or sudamina, on 
the chest and abdomen. J/erpes zoster of the trunk and limbs may 
also occur, mostly in patients with caries of the spine. 


THE SKIN 269 


Pityriasis Tabescentium.—In more or less advanced cases other 
skin eruptions are often seen which are, within certain limits, charac- 
teristic of phthisis. In those who sweat profusely the atrophied skin 
is during the day dry, pale, and brittle, and the upper epidermic layer 
desquamates and sheds yellow or gray scales. In some cases it looks 
as if the skin was covered with dust. It is known as pityriasis tabes- 
centium and. occurs mostly in consumptives who are not extremely 
emaciated, but who have excessive secretion of sweat and sebum; it 
is localized over the chest anteriorly and posteriorly, but at times the 
entire body is covered with it. It may be seen in other wasting diseases, 
but most often in phthisis. 

Pityriasis Versicolor.—This is even more often seen in phthisis. 
The eruption is discretely scattered over the anterior and posterior 
aspects of the thorax, and consists of small macules, slightly raised 
above the level of the skin, round or oval in shape with well-defined 
margins. Scales can bé. scratched off and when examined show 
roundish, shining microscopic spores, the Microsporon furfur. 





Fig. 47.—Papulonecrotie tuberculides. In this patient the eruption occurred on the 
extremities (Darier.) 


The color of the eruption varies in different individuals, but is 
mostly brown, or a dirty yellow, darker in those who lead an outdoor 
life, and over the arms and neck when these are affected, while in 
negroes they are almost white. In patients who neglect to attend to 
the cleanliness of their bodies the macules may coalesce, forming large, 
irregular plaques covering large tracts of skin anteriorly and poste- 
riorly, which desquamate upon scratching. 

It is seen in consumptives who sweat profusely at night, which 
favors the growth of the fungi, and in patients whose skin has a ten- 
dency to scale, which assists in their detachment. Piéry! has inoculated 
guinea-pigs with the scales removed from such patients and obtained 
positive results, and he suggests that it is a tuberculous dermato- 
mycosis. 

When seen on the chest, pityriasis versicolor is fairly indicative of 
phthisis, although it occurs in other cachectic diseases, notably cancer. 


1 Gaz. de hép., 1912, 85, 531. 


‘ 


270 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


Tuberculides.—This term was suggested in 1896 by Darier to 
designate certain skin eruptions which are found in connection with 
tuberculous infection and disease. Of the various types which have 
been classified under this term, only aenitis and folliclis are of special 
interest to those who care for tuberculous patients. 

Acnitis is seen most in adolescent or young adult individuals and 
is found mainly on the face, rarely on the limbs, and genital organs. 
The eruption consists of either small, red, or dark brown, circumscribed, 
and indolent nodules or papules. Each lesion lasts about a month when 
it is either absorbed or, more commonly, it suppurates and opens on 





Fic. 48.—Acnitis in a man aged twenty years. (Darier.) 


the surface leaving a small scar behind. Crops appear one after another 
so that we can always see several of these papules in various stages of 
development symmetrically scattered over the face, and at times over 
the back between the shoulder blades. It is at times difficult to differ- 
entiate these papules from acne, but the absence of seborrhea and 
comedones favors the diagnosis of acnitis. 

Folliclis is also seen in youthful persons, the eruption appearing in 
successive crops on the forearms, hand, fingers, elbows, knees, feet, 
and ears, and rarely on the face. It is not rare on the trunk, especially 
over the shoulder-blades. The papule is dark red, which is within 
about a week transformed into a pustule at the summit. The pustule 


THE SKIN 271 


dries, and finally crusts, and this is shed in a couple of weeks, leaving 
a depressed scar. In nearly all cases we meet with crops in various 
stages of development. 

There seems to be no question that these eruptions are etiologically 
associated with tuberculous infection. But they are mainly associated 
with glandular, osseous, serous, visceral or cutaneous tuberculosis. 
It is also noteworthy that they are mainly found in cases in which the 
just-mentioned tuberculous lesions are either latent, or quiescent, and 
in the numerous cases of pulmonary tuberculosis in which the writer 
has observed folliclis and acnitis, the lung lesions were inactive. Many 
dermatologists, notably Darier,! Jadassohn,? Lewandowsky,’ Stokes,' 
and others, point out that tubercle bacilli are only rarely found in 
sections of the papules, or in the pus, and even inoculation experiments 
prove negative in most cases. The histological structure has been found 
typically tuberculous only in exceptional cases; in most cases it is 
found inflammatory and necrotic. However, it is the consensus of 
opinion that they are due to emboli of tubercle bacilli circulating in the 
blood and which are deposited in the hypersensitized skin, calling 
forth an allergic response. 

Elsewhere in this book (see Chapter XXX) we have shown that 
there appears to be a decided antagonism between tuberculous lesions 
of the skin and the lungs. These dermic lesions seem to confirm this 
observation. All writers, notably Darier, Lewandowsky, and Stokes, 
point out that while most patients have either a family history of tuber- 
culosis, or symptoms of latent tuberculous disease of the lungs, gland 
or bones, the eruption itself runs an afebrile course and constitutional 
symptoms are almost invariably lacking. It is therefore advisable to 
reassure the patient that while cosmetically the disease is a nuisance, 
there is little danger of developing active pulmonary tuberculosis. 
In patients with confirmed phthisis the appearance of acnitis or folliclis 
is an indication of a good prognosis as regards the lung lesion. 

The Hair.— Many authors have stated that alopecia is more fre- 
quent in phthisical subjects than in others, and it has been attributed 
to the same causes as those operative when the hair falls out after an 
attack of typhoid fever, ete. But in my experience this is not true. 
The tuberculous patients in my hospital and private practice are 
not more often bald than others of the same class, nor do I meet with 
many consumptives who have localized alopecia, or alopecia areata. 
Premature grayness of the hair, which Cornet mentions as very fre- 
quent among consumptives, has also not been found by me to be 
frequent in tuberculous patients in the United States. 

Clubbed Fingers.—Clubbed fingers were already mentioned by 
Hippocrates as a symptom of phthisis, and French writers at present 


1 Dermatology, Philadelphia, 1920, p. 563. 

2 Tuberkulose der Haut, Berlin, 1906, 

3 Die Tuberkulose der Haut, Berlin, 1916. 
4 Am, Jour. Med. Sci., 1919, 157, 313, 522, 


272 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


‘all them doigts hippocratiques. They are found in about one-third 
of advanced consumptives, and are probably caused by chronic per- 
ipheral passive congestion. Clubbed fingers are not exclusively met 
with in phthisis, but also in empyema, bronchiectasis, chronic bron- 
chitis, asthma, and pulmonary emphysema, in thoracic aneurysms, 
etc. They have also been encountered in rare cases of cirrhosis of 
the liver, cancer of the lung and amyloid disease. 

In phthisis we usually find that the fingers of both hands are thick- 
ened and bulbous, like a club or drumstick, resembling somewhat 
the condition seen in chronic onychia. The terminal phalanges are 
enlarged, the nails curved longitudinally and laterally. In a recent 
study. Corper, Cosman, Gilmore and Black,! refer to these changes as 

“the hyperconvex nail,’ and they state that it occurred to the extent 
of about 75 to 95 per cent of cases of pulmonary tuberculosis, there 
being no difference in the incidence dependent upon the activity of the 
disease or the sex of the case. In the writer’s experience, the percentage 





Fic. 49.—‘‘Drumstick”’ fingers and curved nails. 


of incidence has been much lower. From roentgenographic studies it 
appears that the bones and joints are not affected, nor is the skin 
altered in any way, but only the superficial soft parts are hypertrophied. 
As to what the change consists in we are in ignorance because of 
lack of anatomical and histological studies. Some rhage suggested that 
it is a fibrous thickening of the innermost layers of the epidermis, as a 
result of prolonged congestion of the capillaries. This may be true of 
some cases, but in those in which the condition develops within a 
few weeks it is doubtful whether this could be the actual anatomical 
change. Corper and his co-workers have found that hypertrophy of 
the soft tissues of the hands and feet of consumptives has a higher 
incidence in the active (about 65 to 80 per cent) than in inactive cases 
(about 45 per cent). 

In most cases the onset is slow and insidious and the patient knows 
nothing about it until the physician calls his attention to the clubbed 


1 Am. Rev. Tuberc., 1921, 5, 357. 


THE SKIN 273 


fingers. But in rare instances, as has already been noted by Trous- 
seau, it comes on very quickly and within a few weeks the fingers look 








Fie. 50.—Clubbed fingers in phthisis. 


like drumsticks. In these acute cases they may be painful, tender, 
and livid. Lividity is also seen in those suffering from pulmonary 


yr 
ed 











Fic. 51.—Changes in the toes in tuberculous osteo-arthropathy. 


emphysema or fibroid phthisis. The nails are curved and look like 
claws. 
18 


274 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


My observations are in agreement with those of Bezancon! that 
clubbed fingers are not met with in all cases of chronic phthisis, as 
some have stated. A large number of consumptives have normal- 
shaped fingers, while some have even long, tapering terminal phalanges. 
Clubbed fingers are encountered almost exclusively in fibroid phthisis, 
pulmonary emphysema with tuberculosis and in those having exten- 
sive pleural adhesions. In other words, whenever clubbed fingers 
are encountered in a case of phthisis we find that the patient is also 








Fic. 52.—Roentgenogram of a hand in a case of clubbed fingers in pulmonary osteo- 
arthropathy with bronchiectasis and pulmonary emphysema. On the tips of the end 
phalanges marked cauliflower formations; bony excrescences on basal portion of some 
phalanges; typical Heberden’s nodes; broadening of the bases of the middle phalanges. 


suffering from dyspnea and dilatation of the right heart. This would 
suggest mechanical disturbances of the circulation, causing peripheral 
venous stasis. Moreover, the prognosis in these cases is quite favor- 
able as regards duration of life, though the outlook as to comfort is 
rather gloomy. 

Hypertrophic Pulmonary Osteo-arthropathy.—In some cases of far- 
advanced tuberculous disease we meet with enlarged hands and feet 
simulating those of acromegaly. These changes in the extremities were 


1 Arch. gén. de méd., 1904, 1, 1663; 2, 3100. 


THE SKIN 275 


first described by Pierre Marie,! and independently by Bamberger? 
The fingers are altogether increased in volume, the nails enlarged, and 
curved transversely and longitudinally, like the beak of a parrot. In 
most cases the metacarpophalangeal region remains normal, but the 
wrist becomes enlarged and deformed, bulging on its dorsal aspect. 
In many cases there is also some deformity of the spine—kyphoscoliosis, 
and the feet may show changes similar to those observed in the wrists 
and hands, especially the toes and tarsus. In the cases that came 





Fig. 53.—Roentgenograms of hand in a case of fibroid phthisis. 


under the writer’s observation there were pains of variable severity, 
in rare instances almost unbearable, and generally intermittent. 
Milder forms of osteo-arthropathic changes are very common in 
tuberculous patients. From a recent study of these changes by Corper 
and co-workers, it appears that the gums are in the majority of cases 
anemic and hypertrophied, and bony processes decidedly thickened, 
more so in the superior maxilla than in the lower jaw. In about 25 
per cent of cases of pulmonary tuberculosis Corper found that the 
hard palate reveals a thickening located in the midline and extending 


1 Rev. de Médecine, 1890, 10, 1. 
2 Wien. klin. Wehnschr., 1889, 2, 226; Ztschr. f. klin. Med., 1891, 18, 193. 


276 SYMPTOMS REFERABLE TO GASTRO-INTESTINAL TRACT 


from the horizontal plate of the palate bone to the foramen of Scarpa, 
situated in the anterior portion of the palatal process of the superior 
maxilla, especially in pronounced cases. The tumor is distinctly 
hard and bone-like to the touch. It is Corper’s opinion that these 
changes in the palate are part and parcel of the general hypertrophic 
osteo-arthropathy, and it is more common in active than in arrested 
cases. This swelling of the hard palate, known as torus palatinus, 
is, however, not found in tuberculous patients more often than in 
healthy individuals. An investigation by Herman Schwatt in my 
clinic at the Montefiore Hospital and the Bedford Sanatorium showed 
that it occurs in about 16 per cent of persons, tuberculous and others, 
and that neither tuberculosis, nor osteo-arthropathy, is a factor in its 
production. 

We are in the dark as to the cause of these changes in the bones 
and joints in chronic pulmonary tuberculosis. As can be seen from the 
roentgenograms (Figs. 52 and 53) clubbed fingers and osteo-arthropathy 
differ in the fact that in the former only the soft parts are implicated, 
the bones remaining practically normal, while in the latter the tissues 
of the bones and joints are hypertrophied and some osteophytes may 
be seen at the line of the joint cartilages. From the studies of Leo 
Kessel,! Edwin A. Locke,? Montgomery,’ Corper,! and others, clubbed 
fingers are the same process as osteo-arthropathy, and merely repre- 
senting an early stage of it. Locke found early proliferative changes 
in the periosteum of the long bones of the forearm and lower legs in 
cases with clubbed fingers of exactly the same type as in hypertrophic 
osteo-arthropathy. Clinically we differentiate these two conditions by 
the fact that in clubbed fingers only the terminal phalanges are enlarged 
while in osteo-arthropathy the wrist is also affected, and the feet 
usually show the same changes, and in addition there is in most cases 
decided spinal deformity. But this does not exclude the identity of the 
two processes if we choose to regard clubbed fingers as the early stage 
of osteo-arthropathy. The former are, however, more common. 

It is important to emphasize that these changes in the extremities 
are found, as a rule, in extremely chronic cases of tuberculosis, espe- 
cially fibroid phthisis. In many, though the pulmonary lesion is 
undoubtedly active, it pursues a slow, sluggish course, the patient 
lasting for many years, and is able to perform light work. This is to 
be considered in connection with the benignity of phthisis in arthritics 
of other sorts, and in those in whom fibrosis is easily formed. This 
point is discussed in detail in Chapter XXX. 


Arch. Intern. Med., 1917, 19, 239. 
Ibid., 1915, 15, 659. 

Jour. Cutan. Dis., 1916, 34, 285. 
Loe. cit. 


- 2 YD 


CHAPTER XIL 


SYMPTOMS REFERABLE TO THE CARDIOVASCULAR AND 
URINARY SYSTEMS. 


THE CARDIOVASCULAR SYSTEM. 


Cardiac Palpitation.— Of the functional cardiovascular disturbances 
in phthisis the most important are palpitation, tachycardia, and hypo- 
tension. They are very often associated, but at times we meet one to 
the exclusion of the other. 

In incipient cases palpitation is mainly met with in young persons, 
especially chlorotic girls. Slight or moderate exertion, excitement, and 
emotional disturbances may cause an attack, or it may occur without 
any obvious provocation. At times it is very pronounced, and is per- 
haps the only subjective symptom which induced the patient to consult 
a physician. Rarely it is very severe and is accompanied by precordial 
pains and distress and by vasomotor disturbances, such as pallor, or 
flushing of the face, sweating, ete. 

I have met with cases in which palpitation preceded all subjective 
and objective symptoms of incipient phthisis. Some are for this reason 
treated for heart disease. As will be shown when speaking of the 
differential diagnosis of phthisis, the syndrome known as _ hyper- 
thyroidism is often mistaken for tuberculosis. The reverse is also true: 
Very frequently the rapid pulse, the tendency to sweating and flushes, 
emaciation, etc., are erroneously considered symptoms of hyper- 
function of the thyroid, or neurocirculatory asthenia, and treated as 
such. A careful examination of the chest, however, will reveal a tuber- 
culous lesion. 

In some instances, especially in young persons, and in women 
during the menopause, symptoms of the hypoasphyaxial syndrome, first 
described by Martinet,! clearly point to urgency to examine the lungs 
carefully. These individuals have more or less cyanosed facies, cold 
and cyanosed extremities, small pulse, vascular hypotension, peripheral 
venous stasis, and venous distention of the visceral organs shown by 
disfunction of the digestive and internal secretory glands. It is this 
class of tuberculous patients who are frequently treated for neuras- 
thenia, hyperthyroidism, neurocirculatory asthenia, etc. On the other 
hand, experience has shown that, as a rule, while these functional 
symptoms may be very severe, the tuberculous lesions in the lungs are 
usually very mild showing slight, if any, tendency to progression. 


od 


1 Diagnostic Clinique, Paris, 1919, p. 744. 


278 SYMPTOMS REFERABLE TO CARDIOVASCULAR SYSTEM 


In all probabilities this is due to the hyperfunction of the thyroid 
which, as will be shown later on (see Chapter XXX), exerts a favor- 
able influence on the course of pulmonary tuberculosis. 

The causes of the palpitation at this stage are not clear. Some have 
been inclined to attribute it to dilatation of the right heart, but we 
meet it in cases in which this organ is normal. Others believe it is 
due to the anemia—low arterial tension—or to sympathetic nerve 
disturbances. The last factor is apparently operative in many cases, 
because we meet it mostly in nervous patients, in young girls and in 
women during the menopause. Compression of the vagus by enlarged 
glands may be the cause in some cases. Of course, the toxemia of 
phthisis exerts a great influence on the heart, inducing fatty changes 
with resulting tachycardia and palpitation. 

Cardiac irritability is seen also in advanced, but quiescent, cases. 
The patient is doing well, has no fever, no cough, and is not emaciated. 
But the least exertion, emotion, or complication, provokes cardiac dis- 
tress which may be-very painful, almost anginal. Here, the palpita- 
tion is, as a rule, due to cardiac dislocation, and occurs more often in 
left-sided lesions. A large cavity in the left lung with pulmonary con-. 
traction has drawn the mediastinum to the left, and the diaphragm 
upward, so that the heart is pushed upward and to the left, and the 
apex beat may be found in the third interspace at the axillary line. In 
some cases of this class there may also be arrhythmia. The palpitation 
is not so pronounced in right-sided dislocations of the heart, not even 
in complete dextrocardia. 

Palyntation has no influence on the course of phthisis, excepting in the 
advanced stages when it 1s due to dislocation of the heart. In the early 
cases we may meet with annoying palpitation in nervous patients who 
are progressively improving. But from the diagnostic standpoint it is 
a symptom of great value. Hirtz said that “when a patient complains 
of palpitation, examine his lungs; and examine his heart when he com- 
plains of dyspnea.”’ While this does not hold good in every case, yet 
it is well worth bearing in mind, especially when dealing with anemic 
youths. In some cases of phthisis we meet with palpitation for a 
day or two before the occurrence of hemoptysis. 

Tachycardia.— Rapid heart action objectively ascertained—which may 
not be known to the patient at all, thus differing from palpitation, which 
is a subjective symptom—is very frequent vn all stages of phthisis. In 
my experience, over 90 per cent of cases of incipient phthisis have 
tachycardia which is usually permanent or, rarely, paroxysmal. It 
is a symptom of phthisis which is not appreciated to the extent it 
deserves, though it is often very helpful in deciding a doubtful case. 

The tachycardia may be of toxic origin. Every elevation of tem- 
perature in phthisis, as in other acute febrile conditions, is accompanied 
by an acceleration in the pulse-rate. But it is often pronounced in those 
running a subfebrile temperature and also in afebrile cases. In fact, 
in tuberculosis the pulse vs accelerated far out of proportion to the height 


THE CARDIOVASCULAR SYSTEM 279 


of the temperature. In most other cases an elevation of 1° F. is usually 
accompanied by an increase in the pulse-rate of about eight beats per 
minute, while in phthisis we often have a temperature of 100° while the 
pulse counts 120 and even more. In fact, in most afebrile cases of 
phthisis the pulse is over 90 per minute and during the morning sub- 
normal temperature tachycardia is not at all rare. Thus tachycardia 
is an early symptom of phthisis and some writers consider it a premoni- 
tory symptom. 

Permanent Tachycardia.—In a large proportion of cases the tachy- 
cardia is permanent and accompanied by subjective discomfort, such 
as palpitation, languor, debility, dyspnea, etc. In others, it is purely 
objective; the patient is hardly aware of its presence. I have observed 
many cases in which the disease was arrested, or even cured, yet the 
tachycardia remained. At times it greatly interferes with the patient’s 
efficiency. But I cannot agree with those who say that in an arrested 
case one cannot feel saf€ as to the continued favorable progress of the 
patient so long as the pulse-rate remains high. I have seen patients 
who have been able to work for a living without much discomfort in 
spite of the rapid heart action. 

One characteristic of the pulse of the consumptive is its instability 
and variability. While resting the rate may be normal, but the slightest 
exertion—a fit of coughing, some emotional experience, a heavy meal, 
or changing from the reclining to the erect posture—may send up the 
pulse-rate to 110 or 120. Faisans maintained that he did not know 
of any disease in which the pulse is as unstable as in phthisis. 

Paroxysmal Tachycardia.—In rare cases we meet with paroxysmal 
tachycardia. The patient feels comparatively well, and, without any 
exciting cause, he is seized with severe palpitation, dyspnea, or even 
orthopnea and cyanosis. Counting the pulse-rate, we find it 150 to 
200 per minute, small, wiry and often irregular. The attack may 
last a few hours, a day or two. In one case the patient got an attack 
while in my office, the pulse going up from 96 to 160, and looked as if 
he was breathing his last. He recovered in two hours. There was 
in my wards at the Montefiore Hospital a young woman who often 
got these attacks. In the beginning the rapid pulse, dyspnea, cya- 
nosis, and prostration suggested the collapse characteristic of 
pneumothorax. Careful search for signs of air in the pleura proved 
negative. She got these attacks at irregular intervals and recovered 
within a few hours or a day. 

After several attacks, which may come on at frequent intervals, 
we may observe signs of cardiac dilatation—the heart gives way and 
the result is edema of the lower extremities, enlargement of the liver, 
etc. Finally, asystole occurs and the patient succumbs. Paroxysmal 
tachycardia is of grave significance and, when occurring several times, 
will ultimately kill the patient during one of the attacks. Instances 
of sudden death are not unknown among tuberculous subjects. The 
cause is frequently heart failure. 


280 SYMPTOMS REFERABLE TO CARDIOVASCULAR SYSTEM 


Causes of Tachycardia.—The causes are obscure. It has been attrib- 
uted to bulbar lesions, to interstitial neuritis of the pneumogastric 
nerve, to myocarditis, ete. Some believe that it is due to compres- 
sion of the vagus by enlarged tracheobronchial glands, but it would 
seem that the effect should rather be a slowing of the pulse-rate, than 
an acceleration. Indeed, considering that the vagus is often pressed 
upon by enlarged glands, it is noteworthy that a slow pulse is exceed- 
ingly rare in phthisis. Other authors have attempted to explain this 
phenomenon by stating that it depends on which part or branch of 
the pneumogastric is affected by the tuberculous process. On this also 
depends whether the stomach or myocardium will suffer. IK. Bohland! 
is inclined to ascribe the tachycardia in phthisis to the small heart 
characteristic of the disease—in order to pump enough blood into the 
system, the heart must beat more often. In the advanced stages of 
phthisis it is due to myocarditis. The tuberculous toxemia alone does 
not explain the tachycardia because it is found often in afebrile patients, 
as was already stated. 

Permanent tachycardia aggravates the prognosis of phthisis, and 
these patients should not be sent to a high altitude. The causes are 
complex and vary with each case. In patients in whom it is of toxic 
origin we may expect improvement as soon as the fever subsides. But 
in many it is caused by compression of the pneumogastric nerve by 
enlarged tracheobronchial glands, or an adherent apical pleura, neuritis 
of that nerve, or reflexly of gastric origin, fibrous degeneration of the 
cardiac muscle, or tuberculosis or hyperfunction of the adrenals, ete. 
When due to cardiac displacement, especially to the left in left-sided 
lesions, it is permanent. 

Arrhythmia is only rarely observed in phthisis, and the prognosis of 
these cases is rather unfavorable. 

Bradycardia.— A slow pulse vs exceedingly rare in phthisis; those who 
see large numbers of these patients occasionally meet one with a 
pulse less than 50 per minute. One patient under my care had a pulse- 
rate of 36 per minute for several months, and only during febrile 
attacks did it rise to 50 or slightly more. But here there was probably 
an organic heart-block. Gueneau de Mussy, who described some of 
these cases, attributed it to irritation of the pneumogastric nerve. 
On the other hand, there are many physicians of large experience who 
have never seen bradycardia in phthisis. From the few cases met by 
me, it appears that the prognosis in phthisis with a slow pulse is very 
good. 

At the terminal stage of far-advanced phthisis we often meet with 
a slow, soft, almost imperceptible pulse which intermits, indicating 
-ardiac failure, or exhaustion. The pulse is also slowed when meningeal 
irritation complicates the disease. 


1 In Brauer, Schréder and Blumenfeld’s Handbuch der Tuberkulose, 1915, 4, 4. 


THE BLOOD 281 


Arterial Hypotension.—The blood-pressure, measured with a 
sphygmomanometer, is lower than normal in the vast majority of 
phthisical patients. It is evidently due to the toxic effects of the 
metabolic processes of the tubercle bacilli, because an injection of 
tuberculin is usually followed by a decided fall in the blood-pressure. 
Sir Douglas Powell says that the large doses of tuberculin which were 
used in the first days of Koch treatment of lupoid and other forms of 
tuberculosis caused severe collapse, and recent writers, like Levy, 
Geisbock, and others, found that even in small or moderate doses, 
tuberculin reduces arterial tension. It has been found that a low 
blood-pressure is an almost constant characteristic of the very early 
stages of phthisis and, when occurring in an adult without any other 
assignable cause, tuberculosis is to be suspected. My own experience 
has brought me to the conclusion that in cases presenting obscure 
symptoms and signs of’ phthisis, when accompanied by a low blood- 
pressure, the diagnosis may be safely made; conversely, I always hesi- 
tate in cases with high arterial tension, excepting in persons over fifty 
years of age. But even in these high pressure is rare in phthisis. 

This hypotension is quite marked in the early stages and becomes 
more accentuated with the progress of the disease. I find that, as a 
rule, cases of undoubted phthisis with a normal or high blood-pressure 
have a favorable prognosis. This is the case with phthisis in persons 
having interstitial nephritis, gout, pulmonary emphysema, syphilitic 
endarteritis, etc.; they all have high blood-pressure, and the prognosis 
is favorable as regards the tuberculous disease. When the blood-pressure 
as low at first but rises gradually, it 1s an excellent indication of vmprove- 
ment; conversely, tuberculous patients with normal or high blood- 
pressure who begin to show hypotension almost invariably also show 
indications of the extension of the process in the lung and the prognosis 
is aggravated. I have not noted in many cases any relation between 
the hypotension of phthisis and the temperature, the pulse-rate, or the 
dyspnea. It is met with in febrile and afebrile cases; in young and in 
the aged. 

It has also been observed by many authors that patients with a 
tendency to hemoptysis have a high blood-pressure which rises before 
the onset of the bleeding. At one time I tested this point in several 
patients but could not confirm it. Many who bled profusely had a 
very low blood-pressure. 


THE BLOOD. 


The Erythrocytes.— Despite the external appearance of anemia 
frequently seen in many phthisical patients in all stages of the disease 
—which has given rise to the expression “great white plague’’—no 
changes in the cytology of the blood characteristic of the disease have 
been found. In fact, it is noteworthy that many patients who look 
pale show an almost normal blood picture. Only in the advanced 
stages, as a rule, is there to be noted a decrease in the percentage of 





282 SYMPTOMS REFERABLE TO CARDIOVASCULAR SYSTEM 


hemoglobin. In many cases, even with high fever, the hemoglobin 
contents remain normal. At. times a polycythemia is encountered, 
but the hemoglobin is not increased under the circumstances. In rare 
instances I have found a decided decrease in the number of erythro- 
cytes, especially during the very early, and very advanced, stages of 
the disease. In some few cases the count was as low as 1,000,000, or 
even less, but the fact that it is so rare shows that it is an accidental 
occurrence, and cannot be considered characteristic of the disease. 
After profuse pulmonary hemorrhages the anemia may be profound, 
but it is remarkable that the blood picture improves very rapidly 
after the cessation of bleeding. 

There is at times noted a decidedly low percentage of hemoglobin 
in incipient cases, even when the erythrocytes are not decreased in 
number. For this reason some authors have spoken of a pseudo- 
chlorotic blood picture. But soon after the patient is placed under 
proper dietetic and hygienic treatment the hemoglobin content of 
the blood improves, as a rule. It may be stated that in many cases 
there is slight diminution in the number of erythrocytes, and a pro- 
nounced diminution in the hemoglobin content, during the incipient 
and far-advanced stages of phthisis. 

From the researches of Limbeck, Grawitz, and others it appears 
that with the advance of the disease, even with the formation of 
pulmonary excavations, the blood picture is very often not deviating 
from the normal. The yellowish pallor, ‘“ ochrodermia,”’ which is so 
frequent at this stage, is not due to alterations in the cytology of the 
blood, so far as can be ascertained. But there is good reason to believe 
that the total amount of blood in the body is less than in healthy 
individuals; that there is a distinct oligemia. This has been ascribed 
to the loss of water through profuse nightsweats, expectoration, and 
often diarrhea, which brings about a higher specific gravity of the 
blood with a concentration of the cells. 

In the far-advanced stages, with hectic fever, often complicated 
by mixed infection, there is, in addition to leukocytosis, a diminu- 
tion in the number of erythrocytes, with a fall in the percentage of 
hemoglobin. 

Leukocytes.—In incipient phthisis the leukocytes are quite normal 
in number and variety. Even in acute cases, so long as there is no 
mixed infection, the leukocyte count is unaffected. Some authors, 
notably Ullom and Craig! in this country, have found a slight leuko- 
cytosis which increases somewhat with the advance of the disease. 
But inasmuch as it only reaches about 11,000 to 14,000 on the average, 
it cannot be considered of any value diagnostically. We quite often 
find that in women the number of white-blood cells oscillates between 
4000 and 15,000 under normal physiological conditions. 

Accumulated evidence is in agreement with the findings of Blumen- 


1 Am. Jour. Med. Sci., 1905, 130, 386. 


THE BLOOD 283 


feldt! to the effect that the total number of leukocytes is somewhat 
higher in the tuberculous than in healthy persons. While an absolute 
leukocytosis may be found in the early stages of the disease, a relative 
leukocytosis is only found in the advanced stages, and it apparently 
runs parallel with the gravity of the tuberculous lesion in the lungs. 
Eosinophiles are diminished in number relatively and absolutely in 
the advanced stages. But even this is an inconstant phenomenon. 
It may be stated that the tubercle bacillus, or its toxin, exerts no specific 
positive chemotaxic influence on the leukocytes, and we are not justi- 
fied in ascribing a typical influence and affinity of the tubercle bacilli 
on the two main varieties of white cells in the blood. 

Gerald B. Webb, G. B. Gilbert, and L. C. Haven? found the blood 
platelets are increased in number in cases of phthisis. Jn tuberculosis 
in guinea-pigs they observed the same phenomenon. They believe 
that the blood platelets either contain or supply opsonins. The fact 
that they are increased at an altitude of 6000 feet would, according 
to Webb, point to a reason for the salutary effects of high climates 
on phthisical patients. 

With the advance of the disease leukocytosis is not rare; it is usually 
transient, but rarely permanent. It appears to depend on the activity 
of the tuberculous process, the intensity of the fever, the presence of 
complications, etc. But there are so many exceptions to this rule 
that it cannot be utilized for diagnostic and prognostic purposes. It 
appears, however, that an injection of tuberculin is usually followed by 
transient leukocytosis. Some have attempted to judge the presence 
of excavation by the white-cell picture, but have failed. Wright’s 
attempt to utilize his tuberculo-opsonic index in the prognosis of 
tuberculosis has also failed to give satisfaction to most authors. 

Arneth’s Blood Picture.—A great deal has been made by some 
authors of Arneth’s blood work in infectious diseases, especially tuber- 
culosis. His theory is based on his observations of the growth of the 
neutrophile and the changes of the nuclei, or granules within these 
cells during the period. He developed a very complicated blood pic- 
ture, based on the number of granules or fragments in each neutrophile. 
His contention is that when the disease takes a bad turn, there is an 
increase in the number of young forms of neutrophiles containing but 
one granule as a nucleus, and a decrease in the older forms of cells 
which correspond to the polymorphonuclears of other writers; he 
calls it a shifting of the blood picture to the left. 

This method has been given a trial by many authors and they, as 
a rule, could find no diagnostic or prognostic hints which were constant; 
in fact, the contradictions were so frequent and notorious that it has 
been abandoned altogether by nearly all who were originally enthu- 
siastic in its favor. 


1 Ztschr. f. exper. Pathol. u. Therap., 1919, 20, 14. 
2 Arch. Int. Med., 1914, 14, 743, 


284 SYMPTOMS REFERABLE TO CARDIOVASCULAR SYSTEM 


Tubercle Bacilli in the Circulating Blood.—That the virus of tuber- 
culosis may be found in the blood has been suspected for a long time. 
As far back as 1866, Villemin withdrew blood from the femoral artery 
of a tuberculous rabbit, and also used blood drawn by leeches from a 
phthisical patient, and injected it into a guinea-pig, and thus trans- 
mitted the disease. Marcet! repeated these experiments in 1867. 
Weichselbaum, in 1884, found tubercle bacilli in the blood of patients 
suffering from miliary tuberculosis, and more recently many authors 
have reported positive findings in patients with chronic, or even quies- 
cent, tuberculous lesions. Liebermeister? found them in 75 per cent 
of cases a week or two before death, and in many early cases of tuber- 
culosis. Some authors, notably Rosenberger,’ Koslow, Kurashige,‘ 
etc., have even stated that in all cases of tuberculosis bacilli may be 
found when carefully looked for, while Klemperer found them in 7 
cases in which the disease was only suspected but could not be diagnos- 
ticated with the usual clinical methods.® 

At one time great enthusiasm was entertained that here we have 
a reliable method for the recognition of obscure tuberculous disease 
by simply ascertaining a bacteremia before the bacilli have had an 
opportunity to settle in some organ and produce gross pathological 
changes perceptible to the clinician. But then still other investigators, 
like Liebermeister, Suzuki and Takaki,® and Kurashige, discovered 
tubercle bacilli in the blood of apparently healthy individuals, and 
Clara Kennerknecht,’ in the blood of 91 per cent of 120 apparently 
healthy children, of which only 68 were tuberculous on subsequent 
observation, and the hopes entertained for the clinical application of 
this method of diagnosis vanished. 

Further investigations by Walter V. Brehm,’ Beitzke, Schern, and 
Dold have shown that there was a source of error which was not 
considered by most of these bacteriologists. The tap water used in 
diluting the blood often contains acid-fast rods which look like tubercle 
bacilli under the microscope (see p. 30). These acid-alcohol-fast rods 
may be bacilli, or some other substances, but they are not pathogenic 
to susceptible animals. It has also been found that fragments of red- 
blood corpuscles may take on the stain of the tubercle bacilli and show 
acid-fast properties. 

The microscopic test proving unreliable, inoculation experiments 
have been made to clear up the problem. The blood of tuberculous 
patients was injected into susceptible animals. Some authors, like 


1 Quoted from Calmette, L’infection Bacillaire, p. 216. 

2 Virch. Arch., 1909, 197, 332; Med. Klinik, 1912, p. 798. 

3 Am. Jour. Med. Sci., 1909, 137, 267. 

4 Ztschr. f. Tuberkul., 1911, 17, 347; 1912, 18, 430. 

5 For a résumé of the literature on this subject, see, Lowenstein, Vorlesungen tiber 
Tuberkulose, Jena, 1920, pp. 146-164. 

6 Zentralbl. f. Bakteriol., 1910, 61, 149. 

7 Beitr. z. Klinik. d. Tuberkul., 1912, 23, 265. 

8 Jour. Am. Med. Assn., 1909, 53, 909. 


THE URINARY SYSTEM 285 


Anderson,! Rumpf,? Ravenel and Smith,? Querner,! Leo Kessel,> and 
others, were either entirely negative, none of the animals experimented 
on showed any tuberculous lesions after death, or only a few of them 
were infected. Liebermeister, on the other hand, reported that in 6 
cases the animals were infected with tubercle bacilli in the blood of 
human beings who showed no clinical symptoms of the disease. 
Investigations by Mildred C. Clough® showed that inoculation tests 
are unreliable, especially when the blood is drawn from patients suf- 
fering from chronic phthisis. She collected from the literature 1508 
cases studied by guinea-pig inoculation, of which 195, or 12.9 per cent, 
gave positive results. In 500 cases Frankel’ found 20 per cent positives; 
Fischer® in 1250 cases, 17 per cent. However, in all these cases acute 
and chronic tuberculosis were indiscriminately mixed together. In 48 
cases of miliary tuberculosis, 66.6 per cent gave positive results. In 
other words, according to Clough, only 6.7 per cent of chronic cases, 
and 66.7 per cent of acute cases give positive results to inoculation 
tests. Miss Clough says that with blood cultures positive results are 
more often obtained of the existence of a bacteremia in tuberculosis. 
The reason why tubercle bacilli in the circulating blood are only 
rarely pathogenic to susceptible animals has been given differently by 
different authors. Some maintain that it all depends on the number 
of bacilli in the injected blood, and when they are scarce, they may 
prove ineffective. Moreover, while inoculating the blood not only 
bacilli are injected, but also antibodies, and that the bacilli, while 
remaining in the living blood, have been attenuated in their virulence. 
If their parilenee had been maintained, acute miliary tuberculosis 
would have resulted in the patient from whom the blood was drawn. 
Irom the theoretical viewpoint it is important to mention that it 
is agreed that while circulating in the living blood tubercle bacilli do 
not Binhaoly by proliferation, it is only when they settle on some 
susceptible tissue that they may grow in number thr ough multiplica- 
tion. 
So far, the finding of tubercle bacilli in the blood is of no diagnostic 
or prognostic value, even in suspected cases of acute miliary tuber- 
culosis. 


THE URINARY SYSTEM. 


The Kidneys.— There appear to be no changes in the structure and 
functions of the kidneys which can be considered specific and char- 
acteristic of early phthisis, excepting in cases with a very acute onset, 


1 The Presence of Tubercle Bacilli in the Blood in Clinical and Experimental Tuber- 
culosis, Hygienic Laborat. Bull., Washington, 1909, No. 57. 

2 Miinchen. med. Wehnschr., 1912, 59, 1951. 

3 Jour. Am. Med. Assn., 1909, 53, 1915. 

4 Miinchen. med. Wehnschr., 1913, 60, 401. 

5 Am. Jour. Med. Sci., 1915, 150, 337. 

6 Am. Rev. of Tubercul., 1917, 1, 598. 

7 Schmidt’s Jahrbiicher, 19138, 217, 2056. 

8 Ztschr. f. Hygiene, 1914, 78, 253. 


286 SYMPTOMS REFERABLE TO CARDIOVASCULAR SYSTEM 


with high fever, which affects these organs in the same manner as 
hyperthermia due to other causes, or in cases in which the kidneys are 
inoculated at the onset together with many other organs, as in acute 
miliary tuberculosis. Recent investigations of the renal function by 
Charles W. Mills! and John T. Henderson, and also by Elmer H. Funk,? 
show that in the incipient stage it is normal, and that it is reduced 
in the advanced stages of the disease only when there is evidence of 
structural damage to the kidney. 

Some writers, notably the French, have described polyuria, phospha- 
turia and albuminuria as very frequent in early and even in latent 
phthisis. Barbier’ says that albuminuria is often the only sign observed 
for a long time before other symptoms make their appearance; and 
that this albuminuria is often misunderstood by physicians. Albert 
Robin‘ describes pretuberculous polyuria: The quantity of urine in 
the early stage is increased; in the second stage normal; and in the 
third stage diminished, although some patients have polyuria through- 
out the course of the disease. The oliguria of the advanced stage is 
closely related to the fever, sweats, and eventual diarrhea. Robin 
maintains that the polyuria of early phthisis is simple, showing no 
abnormal constituents, or, at most, there may be phosphaturia,when, 
at times, it may be severe enough to cause irritation of the kidney 
substance, congestion, and, finally, albuminuria. 

These changes have, however, not been met with sufficient constancy 
to place them in the category of pathognomonic or specific symptoms 
of early tuberculosis. Among 100 cases of early tuberculosis that I have 
especially investigated for the purpose of testing this point, I found 
albuminuria in only 9 cases and casts in only 3. 

Albuminuria in Advanced Cases.—In the advanced stages albumin- 
uria is very frequent. Montgomery found albumin present in about 
one-third of cases of phthisis. In the majority of cases the amount 
was only a trace and when found in larger amounts it was always asso- 
ciated with casts and blood or pus. By using delicate methods Mills 
and Henderson found traces of albumin, with or without hyaline casts, 
in 40 per cent of sanatorium patients. It appears that cases with 
intestinal ulcers have larger amounts of albumin than others. From 
his studies Montgomery arrives at the conclusion that a large number 
of casts in the urine of consumptives are indicative of an unfavorable 
prognosis, and the reverse. 

As to the causes of the albuminuria we are not clear. Some look upon 
it as caused by the irritation of the tuberculous toxins, which are elimi- 
nated with the urine, on the renal parenchyma, while others see in it 
the effects of the chronic fever, or actual tuberculosis of the kidneys. 
In an exhaustive study of the problem, N. Leon-Kindberg® arrives at 


1 Am. Rev. Tuberc., 1917, 1, 574. 2 Thid., 1918, 1, 145, 
3 Brouardel and Gilbert’s Traité de Médecine, Paris, 1910, 29, 423. 

4 Traitement de la tuberculose, p. 498. 

6 Etudes sur le rein des tuberculeux, Paris, 1913. 


THE URINARY SYSTEM 287 


the conclusion that the so-called “tuberculotoxins” cause no lesions 
in the kidneys. The presence of isolated tubercles in the kidneys 
explains perhaps some cases of bacteriuria. 

It must be mentioned that mixed infection, such as is seen in pul- 
monary cavities containing, in addition to tubercle bacilli, also pyogenic 
microorganisms, is usually the cause of albuminuria in the advanced 
stages of phthisis where there is no concomitant renal tuberculosis. 

Nephritis in the Course of Phthisis.—Symptoms of acute nephritis 
are very rarely met with during the course of phthisis; but the 
chronic forms, parenchymatous and _ interstitial, have, however, 
been found in variable proportions. Bamberger found nephritis to- 
gether with phthisis to the extent of 15 per cent; Potain states that 
one-fifth of all consumptives have nephritis; and others have found 
even higher percentages. Senator was inclined to the opinion that 
tuberculosis is an important etiological factor in chronic parenchy- 
matous nephritis. But it appears that clinical symptoms of nephritis 
are usually altogether absent, even when albumin and casts are found 
in the urine, and cardiac hypertrophy is exceedingly rare. 

Most of these views are based on the presence of albumin in the 
urine, and Montgomery! has shown that in pulmonary tuberculosis 
albumin and casts are not often associated with evidences of nephritis. 
In phthisis, albuminuria is not necessarily a manifestation of nephritis, 
or even of renal tuberculous lesions; but in many cases, especially in 
fibroid phthisis and emphysema, it is due to cardiac dilatation, to 
intestinal and hepatic disturbances, etc., which are so frequent in 
advanced phthisis. Albuminuria may also be the sole indication of 
a tuberculous lesion in a kidney which manifests itself by no other 
symptom during life. Thus, in a painstaking study of 106 pairs of 
kidneys taken from consumptives, made by J. Walsh,? 53.9 per cent 
were found to contain tubercles. He also found that among these 106 
pairs of kidneys only 10 showed chronic interstitial nephritis, while in 
44 kidneys from patients suffering from other chronic diseases, there 
were 23 with this form of nephritis, which clearly indicates that tuber- 
culosis of the lungs is antagonistic to the ordinary chronic general 
interstitial nephritis, just as it appears antagonistic to general sclerosis 
of other organs. 

The Amyloid Kidney.—In the far-advanced stages of phthisis with 
large suppurating cavities in the lungs, we often encounter amyloid 
degeneration of the kidneys, as in suppuration due to other causes. It 
is usually found associated with amyloid changes in other organs, 
notably the liver, spleen, and intestines. But even this is not as fre- 
quent as would be expected. White found 9.2 per cent; Walsh 6.6 
per cent, and he never found it exclusively in the kidneys; Blum in 
only 6 per cent, but he points out that 79.2 per cent of all amyloids 
were caused by tuberculosis, of which 54.4 per cent is pulmonary 
phthisis. 

1 Fourth Annual Report Henry Phipps Institute, 1908, p. 120. 
2 Tr. Sixth Intern. Congr. Tuberc., 1908, 1, 347. 


288 SYMPTOMS REFERABLE TO CARDIOVASCULAR SYSTEM 


Its symptomatology is that of amyloid disease of the liver and intes- 
tines, and because it is always associated with other changes in the 
kidneys, such as chronic parenchymatous nephritis, the resulting 
symptoms are always complex. Albumin is usually present in the urine. 
I find it safe to conclude, when the liver is enlarged and there is pro- 
fuse diarrhea, that there is no doubt that the kidneys are amyloid. 
But when there is no diarrhea, there is polyuria of low specific gravity, 
casts, and but little albumin. 

Terminal Edema.— Kdema is present in a large proportion of cases 
of advanced phthisis; the ankles and knees especially are thus affected 
during the terminal stages, but it does not always depend on the con- 
dition of the kidneys. Montgomery found no relation between edema 
and the occurrence of albumin ‘and casts in the urine, and suggests 
that the edema found in tuberculosis does not depend primarily on 
nephritis. General anasarca is at times seen in far-advanced cases 
toward the end, and this may be a manifestation of the state of the 
kidneys, but when we bear in mind that in these cases we also have 
cardiac dilatation, it is clear that the pathogenesis is often complex. 

The edema may be considered an ill omen, and I have not seen a 
consumptive with edematous ankles and knees survive, or even 
improve. It may be unilateral, sometimes one-half of the body is 
swollen and pitting, corresponding to the side on which the patient 
lies. At times we see it only in one upper extremity, due to pressure 
on the veins coming to the arm by tuberculous glands, or when they 
are implicated in the adhesive pleurisy of that side, and more com- 
monly by thrombosis of the innominate, subclavian, or other veins. 
Phlebitis or thrombosis of the femoral, popliteal, and crural veins is 
even more frequent (see Chapter X XIX). 

Uremia.—Symptoms of uremia are not often met with in phthisis, 
but not so rarely as some authors would lead us to believe. In the 
advanced stages we meet at times with typical uremia, which is often 
mistaken for meningeal infection. I have seen several cases of convul- 
sions due to this cause. In severe dyspnea without fever, arising 
suddenly, uremia is to be thought of in cases with albumin and casts 
in the urine. Often the diarrhea observed in these cases is distinctly 
of uremic origin, and at times we meet with pulmonary edema. These 
conditions are usually very difficult of recognition and differentiation. 


CHAPTER XIII 
NERVOUS SYMPTOMS OF PHTHISIS. 


As an exquisitely chronic disease, phthisis is accompanied by many 
morbid manifestations of the nervous system; in fact, nearly every 
symptom of the disease is often influenced by the effects of the tuber- 
culouf$ toxins on the nervous system. The neurotic phenomena may 
make their appearance immediately at the outset, in some they pre- 
cede the actual onset of active phthisis, while most confirmed con- 
sumptives have a psychology peculiarly their own, and show symptoms 
of nervous aberration which cannot escape the vigilance of the obser- 
vant physician. 

Neurasthenia and Psychasthenia.—The onset of phthisis is often 
accompanied by symptoms simulating that syndrome which is known 
under the vague term of neurasthenia; indeed, many patients have 
been treated for neurasthenia for months before the true nature of 
their affection was recognized. These symptoms have been described 
by many authors and deserve careful consideration. 

A large proportion of incipient and confirmed consumptives complain 
of vertigo, headache, pains along the spine, irritability of temper, 
insomnia, not necessarily due to nightsweats, and fleeting pains of the 
chest which, at times, cannot be attributed to circumscribed pleurisy; 
frequent attacks of tachycardia, irrespective of the temperature and 
cardiac palpitation, are not rare. There is also the characteristic 
languor and persistent weariness, which is not relieved by sleep; on 
the contrary, many state that they feel weary and tired in the morn- 
ing, on getting out of bed, and that this tired feeling wears off in the 
afternoon or evening, all of which is suggestive of neurasthenia and 
psychasthenia. Considering these symptoms there is little wonder that 
many patients are treated for “nervousness” until an attack of dry 
or moist pleurisy, or of hemoptysis, or a careful examination of the 
chest, reveals the true state of affairs. Papillon! goes so far as to say 
that he suspects every victim of neurasthenia to be a subject of latent 
tuberculosis, and G. D. Head? believes that a considerable propor- 
tion of neurasthenics harbor a tuberculous infection which is so con- 
cealed that it escapes detection by the usual clinical methods. Con- 
sidering that neurasthenia is quite often the result of toxic causes, it 
is clear that tuberculous toxemia may be a cause of these symptoms 
in many cases. If the chests of all patients treated for neurasthenia 


1 Arch. de Scien. Méd., 1900, 5, 19. 
2 Jour. Am. Med. Assn., 1914, 63, 996. 


19 


290 NERVOUS SYMPTOMS OF PHTHISIS 


were carefully examined, a large proportion of phthisis which is now 
only recognized in the advanced stages would be identified at earlier 
stages. 

Reflex Nervous Phenomena.— Aberrations of the sympathetic or para- 
sympathetic nervous system are not rare in phthisis. Among these may 
be mentioned the unilateral flushes of the face and occasionally of one 
ear, combined with a feeling of warmth, sweating, etc. In some cases 
it has been observed that the cutaneous temperature is higher on one 
side of the chest. These unilateral symptoms are usually found on the 
side corr esponding to the affected hemithorax, and in bilateral lesions, 
to the side in which the recent, or more active, lesion is located. In 
some patients with extensive excavations in the lung, the nostrifcor- 
responding to the affected side is widely dilated. Dermographism 
is very frequent. 

These disturbances in the autonomic system have, during recent 
years, been studied by many authors. Meyer Solis-Cohen! looks upon 
them as a defense reaction of the internal secretory organs to the 
tuberculous toxemia. D/’Oelsnitz and Cornil® attribute them to irri- 
tation of the cervical sympathetic and found that they can be best 
detected by the oscillometer. They suggest the oscillometer, applied 
to the arm corresponding to the affected side, as a useful diagnostic 
measure to supplement routine diagnostic methods for the detection 
of latent intrathoracic lesions. Ernst P. Boas,’ who studied the prob- 
lem with the Goetsch epinephrin test, arrives at the conclusion that the 
functional disturbances of the circulatory, alimentary, and nervous 
systems in the tuberculous are not specific manifestations of tubercu- 
losis, but are usually conditioned by a constitutional nervous instability 
of the patient. At times they may appear without such an underlying 
predisposition, and then they may bear some relationship to hyper- 
activity of the thyroid. When latent, these vasomotor and other 
functional disturbances, may be activated by tuberculous infection, 
and they appear to belong to the same group as, and are analogous to, 
those of neurocirculatory asthenia. 

An important symptom of phthisis is dilatation of the pupils, to which 
Rogue,’ Destrée,> and also T. F. Harrington’ drew attention. Har- 
rington described the widely dilated pupils as “not a paralyzed pupil, 
but rather one which seems to be in a more or less constant state of 
dilatation, due to some irritation along the track of the nerve fibers in 
the celiospinal region,” and says that they may be found in cases before 
the evidences of active disease can be discovered. Dilatation of 
but one pupil is more frequent, some authors saying that it occurs in 
more than 50 per cent of cases; that it is an early symptom and may 
Am. Rev. Tuberc., 1917, 1, 289. 

Bull. de la Soe. des Hép. de Paris, 1919, 48, 861. 
Am. Rev. Tuberc., 1920, 4, 455. 
Gaz. méd., de Paris, 1869. 


Jour. de méd. et de pharm., 1894, 241. 
Boston Med. and Surg. Jour., 1899, 151, 575 


an mk wo mS 


PAINS 291 


be found before other symptoms and signs make their appearance. 
More recently, Meyer Solis-Cohen, Emil Sergent,! and H. Saint- 
Aude’ have given this symptom attention. Sergent has shown that this 
sign is not peculiar to syphilis, but that it is very frequently encoun- 
tered in pleuropulmonary tuberculous lesions and especially in chronic 
phthisis. He distinguishes several varieties. The inequality may be 
an isolated phenomenon, and the abnormal pupil is on the same side 
as the affected lung. It may also be a part of an oculopupillary syn- 
drome, myosis being accompanied by diminution of the palpebral 
fissure and retraction of the eyeball on the affected side. In some 
cases the inequality of the pupils not only forms part of the oculo- 
pupillary syndrome, but is also accompanied by vasomotor symptoms 
in the cheek and ear on the same side. Instead of myosis of the pupil 
on the side corresponding to the affected lung, there is mydriasis with 
vasomotor symptoms, but without the oculopupillary syndrome. It 
is mainly seen in cases of phthisis in which the apical pleura is involved 
in the process, and in apical pleurisy. In most cases of this type there 
is also found some swelling of the supraclavicular glands (see p. 486). 
It is due to irritation of the cervical sympathetic by the inflammatory 
process in the lung apex and pleura. With the improvement in the 
disease the difference in the pupils may disappear, but I have seen it 
persist after the patient recovered. At times, one pupil is unduly 
contracted. 

Muralt* pointed out that these unilateral nervous phenomena may 
be observed within certain limits experimentally after the induction 
of therapeutic pneumothorax. He found that with the increase in the 
intrapleural pressure, the pupil dilates and the cheek flushes on the 
affected side, and in some cases there are typical attacks of migraine, 
while with the decrease in the pressure the phenomena disappear. 

Pains.— While a large proportion of tuberculous patients pass 
through the disease painlessly, there are many who suffer from pains 
and aches of various degrees of severity. The pains may be in any 
part of the body, but the most characteristic are those of the chest 
and upper extremity. Kuthy found that among 650 patients, 60 per 
cent had pains in the chest, and of these it was localized in 85 per cent 
in the affected, or more affected, side. 

Many of my patients have received the first intimation of trouble 
with their lungs through pains which were usually felt in the infra- 
clavicular space above the second rib, and more often in the supra- 
spinous fossa, between the shoulder-blades, or under them. It is 
usually of a dull character, uninfluenced by motion, breathing or 
coughing, worse during the night. The skin over the affected area 
is only rarely tender, but deep pressure almost invariably aggravates 
it; tapping this region may bring on a coughing spell. Hyperesthesia 
of the spine between the shoulder-blades is quite common. 

1 Ann. de Méd., 1917, 4, 140; Progress Médicale, 1912, 28, 234. 


2 Thése de Paris, 1917-18, No. 63. 
3 Mediz. Klin., 1913, 9, 1814 and 1901. 


292 NERVOUS SYMPTOMS OF PHTHISIS 


In more advanced phthisis pains in the shoulder may be actually 
agonizing, worse during the night, depriving the patient of his sleep, 
and resisting all therapeutic efforts at relief. When occurring in the 
incipient state they are not so acutely felt, but may extend all along 
the arm and forearm down to the finger tips. Minor exposures to the 
vicissitudes of the weather may bring about pains, and the patient then 
believes that he is affected with rheumatism. In fact, many cases 
of “rheumatism”’ of the shoulder turn out to be phthisis. Diaphrag- 
matic pains are frequent. They are described by the patients as stab- 
bing in character, or as if there was a wound in that region, and are 
usually due to pleural adhesions, and may be aggravated by deep 
breathing, coughing, and sneezing. 

Hyperesthesia is very rare in phthisis unless there is complicating 
pleurisy. The pains are usually elicited by pressure on the regional 
muscles over the affected parts of the lungs. When the apex is affected, 
the sternocleidomastoidei and the trapezii may be painful; when the 
lesion is more extensive the scaleni, pectorales, and intercostals, and 
when there is a lesion at the base, the lumbar muscles may be painful 
on pressure. In pleurisy there are hyperesthesia and hyperalgesia (see 
p. 483). These pains are not due to cough because they are unilateral. 
They are accompanied by spasmodic contractions of the regional 
muscles, caused by reflex irritation of the supplying nerves. 

These pains have been studied very carefully by Henry Head,! 
Sir James Mackenzie,? and more recently in this country by Lovell 
Langstroth.? Head found that these pains were either local or referred, 
and when due to pleurisy they coincided precisely with the situation of 
the pleural area involved, and were accompanied by deep tenderness, 
but not by superficial hyperalgesia. In cases of phthisis marked by 
successive acute or subacute attacks, involving previously healthy 
parts of the lung, referred pains were mostly found. He attributed 
them to the fact that the end-organs of the sensory nerves in the por- 
tion of the lung invaded remained intact, and capable of conveying 
impressions when irritated. These nerve endings were destroyed after 
the disease advanced, causing necrosis, and were no more capable of 
causing referred pain. Superficial tenderness is particularly liable to 
spread along the paths of the nerves, and Head believed it due to the 
cachexia and pyrexia characteristic of each acute exacerbation of the 
disease. Within certain limits, he was able to determine the lung area 
involved by the cutaneous hyperalgesia. A review of the various forms 
of pains in phthisis is given by F. Jessen‘ in a special monograph. Clini- 
cal experience has taught, however, that Langstroth’s conclusion to 
the effect that this hyperalgesia is practically of no importance in 
diagnosis, or in localizing pulmonary lesions, is correct. But in the 


1 Brain, 1896, 19, 153. 

2 Symptoms and Their Interpretation, London, 1909. 

3 Arch. Int. Med,, 1915, 16, 149. 

4 Lungenschwindsucht und Nervensystem, Jena, 1904. 


PAINS 293 


diagnosis of pleurisy, especially of the diaphragmatic portion of the 
pleura, a study of the referred pains is of universal diagnostic impor- 
tance (see p. 483). 

It appears that the tenderness found in active phthisis is the result 
of the rigid contraction of the muscles—an attempt on the part of the 
muscles to protect the diseased viscera beneath them. It is replaced 
by muscular atrophy in the later stages of phthisis. 

The origin of the various pains in phthisis is not always clear. It 
has been shown by Sir James Mackenzie that the lung is insensitive 
to stimulation when healthy or diseased, as is evident from the fact 
that when an exploring needle penetrates the lung the patient feels no 
pain. In fact, no form of stimulation of lung tissue seems to be capable 
of producing sensation, directly or reflexly. It is for this reason that 
necrosis of lung tissue, as it occurs In gangrene, abscess, or tuberculous 
cavity formation, is usually painless. 

The suggestion that the pains in phthisis, as well as in pleurisy 
and pneumonia, are due to pleural involvement does not hold either, 
because the pleura is insensitive. Mackenzie states that he repeatedly 
explored the pleural cavity for any evidences of sensation and could 
employ no form of stimulation capable of producing pain. When 
inducing therapeutic pneumothorax I have repeatedly observed that 
entering the parietal pleura with the needle produced no pain, nor 
does scratching the visceral pleura with the point of the needle produce 
any sensation. Mackenzie is therefore inclined to attribute pains 
of the kind mentioned above to contraction of the overlying muscles. 
This is the reason why no hyperesthesia of the skin is met with in 
phthisis, but pressure pain is frequent. It is due to a visceromotor 
reflex, and occurs along the distribution of the sensory nerves which 
are stimulated by the lesion. The above-mentioned pain in the shoulder 
can be explained by irritation in diaphragmatic pleurisy of the phrenic 
nerve which conducts the stimulus to the skin of the shoulder. Both 
the phrenic and fourth cervical nerves leave the spinal cord at the 
same segment, and the former nerve conducts afferent fibers, as well as 
efferent (motor), and it is in all probability by the former that the 
stimulus is conveyed to the center of the fourth cervical nerve in the 
cord. Pottenger also attributes these shoulder pains to an inflammation 
of the nerve resulting from the reflex segmental stimulation—a true 
neuritis. On the other hand, investigations by Capps! seem to indicate 
that irritation of the central part of the diaphragmatic pleura gives 
referred pain in the neck; and irritation of other parts also gives rise to 
true referred pains, set up by impulses carried to the third and fourth 
cervical segments by the phrenic nerve, and thence to the areas of 
these segments. This point is discussed in detail in Chapter X XVI. 

During the last few days of life the reflexes are usually abolished 
in the phthisical, and they are relieved from all pains; in fact, at times 
we find them very hopeful because they feel no more pains. 


1 Arch. Int. Med., 1911, 8, 717. 


294 NERVOUS SYMPTOMS OF PHTHISIS 


Psychic Traits.—Psychoses met with among tuberculous patients 
may be considered in the main as coincidences, because so many people 
suffer from phthisis, and, inasmuch as this disease is no bar against 
mental alienation, it is but natural that some should become insane 
from any of the causes of this aberration. It is a fact that an enormous 
proportion of insane die from phthisis—Clouston! states that two- 
thirds of deaths among idiots result from tuberculosis—but this may 
be due to their irrational mode of life, as well as to their confinement 
in institutions. Delirium is also very often seen in the terminal stages 
of phthisis and, when not due to meningeal complication, it does not 
differ from the delirium seen in inanition, exhaustion, or febrile intoxi- 
cation due to other causes. But in addition to these occasional psychic 
disturbances, which might be expected, there have been noted other 
psychic peculiarities in phthisical patients, and many authors have 
spoken of a characteristic psychology of the consumptive. 

These phenomena have been observed also in infants. Combe? is 
in agreement with other authors that the tuberculotoxins act on the 
nervous system of infants, as of older children, and cause a decided 
change of character. The infant loses its gayety; it never smiles, but 
cries without cause. It sleeps badly, awaking often, but is difficult to 
arouse in the morning. This change in character is mostly observed in 
children with tuberculous meningitis, but is also seen in those suffering 
from other forms of tuberculosis. 

Many tuberculous patients show a remarkable change in their mental 
traits and character, a disturbance in their emotional life and a striking 
divergence from their previous customs, habits, affections, and tastes. In 
some, this change precedes the evident onset of the disease, in many 
it appears synchronously with the symptoms of active disease; it may 
ameliorate with each improvement, and aggravate with each acute 
exacerbation. 

This change in character manifests itself in various other ways: 
Liberal persons may become stingy and misanthropic, brave ones 
become cowardly, etc. Engel* points out that the original, innate 
temperament or character of the individual becomes strikingly pro- 
nounced in the chronic consumptive: The pessimist suffers from 
marked despondency; the optimist becomes unreasonably hopeful of 
the ultimate outcome, etc. These phenomena may be explained by 
the discordance between the subjective feelings of the patient who is 
not as disabled as the objective findings of the physician would lead 
to expect. The mental make-up of the patient depends greatly on 
his physical condition which, in tuberculosis, is subject to great oscil- 
lations; aggravations and improvements coming and going quite 
unexpectedly. The mental traits per se do not change, but such traits 
as were characteristic during youth, but, as a result of education, 


1 Allbutt’s System of Medicine, 8, 307. 
2 Le, Nourisson, 1916, 4, 73. 
3 Miinchen. med. Wehnschr., 1902, 49, 1383. 


EUPHORIA AND EUTHANASIA 295 


training, and the vicissitudes of life, have been suppressed, reappear 
boldly, unhindered by conventionalities. 

A psychic trait of the consumptive which has been noted by most 
writers is selfishness. He becomes egotistical and egocentric. He is 
interested in the welfare of but one person—himself—to the exclusion 
of all who had depended on him before. He will eat costly food 
while his children starve; he will make unreasonable demands on his 
relatives and friends and show no gratitude. In sanatoriums this has 
been the most important problem with which the officers have to cope, 
and the failure of many superintendents is due to their lack of appre- 
ciation of this trait of the consumptive. As Saxe! states, the ascendence 
of selfishness plays the most important role in the molding of the 
mental traits of the tuberculous. In some patients these factors are 
so pronounced that they completely reveal the concealed elements of 
their characters. “They are whimsical,” say Smith Ely Jelliffeand Elida 
Evans,” “have no sense of responsibility and often do not hesitate to 
spread infection. The nature of many adults suffering from clinical 
tuberculosis is that of a child, selfish, self-centered, irritable, easily 
angered, capricious with their food, will eat only what they like, eating 
irregularly, and appearing underfed. . . . Their strong infantile 
reactions, in that they utterly disregard others, are egotistical, dissatis- 
fied and ungrateful.” O. Amrein® speaks in a similar vein. 

Euphoria and Euthanasia.—Optimism, despite many evidences of 
progressive disease which saps the body, is frequent; only a copious 
hemorrhage, or, more rarely, a spontaneous pneumothorax, will terrify 
the average tuberculous patient. Otherwise, all the symptoms amount 
to little or nothing. An increase in the cough is due to a “cold”; 
anorexia is caused by bad food, ete. 

Barring the functional neuroses, there are no diseases in which 
suggestion—auto- and heterosuggestion—is so effective in modifying 
the course of the malady or in relieving symptoms. An injection of 
water will induce sleep, relieve pain, cough, etc., and even produce 
an increase in temperature exactly like that of the tuberculin reaction. 
In many European sanatoriums there is a routine measure before 
applying tuberculin for diagnostic purposes, to inject water with a 
view of ascertaining whether the fever is due to psychic effects, or to 
the tuberculin. It has been found that 20 per cent of patients react 
to the injectio vacua. Some physicians have been able to suggest the 
hour of the day when the reaction will appear, as well as any, or all, 
of the symptoms which make up the typical tuberculin reaction. The 
effects of this high susceptibility to suggestion are seen in phthisio- 
therapy; quack doctors and remedies are thriving on consumptives 
more than on any other class of patients, excepting perhaps the 
venereal, in whom the element of secrecy is of importance. 





1 New York Med. Jour., 1903, 78, 211 and 263. 
2 Am. Rey. Tuberc., 1919, 3, 417. 
3 Corr.-Bl. Schweitzer Aerzte, 1919, 49, 1300. 


296 NERVOUS SYMPTOMS OF PHTHISIS 


The proverbial euphoria and euthanasia of the consumptive, which 
have been described in such great detail by many medical authors, and 
which have not escaped the attention of writers of fiction who are alert 
for strong dramatic effects, are other manifestations of the proclivities 
to autosuggestion. Experience has taught that when a patient with 
excessive excavations in the lungs, running high fever, and presenting 
other symptoms and signs of this condition, begins to believe that he 
has improved, that he “feels fine,’ has no pains, does not cough 
distressingly, we may look for a speedy relief of the unfortunate by 
that greatest of benefactors for these desperate sufferers, death. It 
is often astonishing to behold the sinking man making plans for the 
future, engage in new enterprises, plan long voyages—not for a cure, 
which he believes he has almost attained, but for pleasure—or, as I 
have seen, arranging for his marriage a few days before his death. 

Very often this optimism and euphoria are excellent aids in our 
attempts at curing these patients. It is a well-known fact that there 
is hardly any hope for a despondent consumptive. On the other 
hand, this euphoria is occasionally harmful because it misleads the 
patient and he neglects the instructions of his physician. 

It appears that as a result of the prolonged state of intoxication 
produced by the absorption of the poisons resulting from the metab- 
olism of the tubercle bacilli, as well as of the products of decom- 
position of the affected lung tissue, the consumptive is in about the 
same mental state as those who are under the influence of mild alcoholic 
intoxication. The external appearance of the consumptive betrays 
his state of intoxication. His bright eyes with dilated pupils, which 
are at times contracted unilaterally, the flushing cheeks, the keen 
intellect which is so often met with among those who before the 
onset of the disease were rather dull in this respect, coupled with a 
flickering intelligence which brightens up suddenly for a few hours, 
but is soon followed by mental depression or fatigue, bear close resem- 
blance to the average person who is under the influence of moderate 
doses of alcohol, or a narcotic drug. 

In tuberculous patients, particularly young talented individuals, it 
is noted that for a few weeks or months, now and then, they display 
enormous intellectual capacity of the creative kind. Especially is 
this to be noted in those who are of the artistic temperament, or who 
have a talent for imaginative writing. They are in a constant state of 
nervous irritability, but despite the fact that it hurts their physical 
condition, they keep on working and produce their best work. This 
spes phthisica has been described by many authors, notably by J. B. 
Huber! and A. C. Jacobson? in this country. They maintain that 
“the quality of genius may, in some cases at least, be affected by 
tuberculosis,’ and that the intellectual powers of the genius are 
quickened by reason of the general psychic excitation resulting from the 


1 Consumption and Civilization, Philadelphia, 1906. 
2 Interstate Med. Jour., 1914, 21, 341. 


INSOMNIA 297 


action of the tuberculous by-products. “They astonish everybody,” 
says Létulle,| “with their mental and intellectual activity; their 
memory, their quick judgment, their delicate reasoning powers are of 
incomparable amplitude.” 

The long list of great writers and artists given below,? to which many 
more may be added, shows that tuberculosis is rather frequent among 
talented individuals, and suggests that the disease may be enhancing 
their productivity instead of reducing it as would be expected a priort. 

Insomnia.—Insomnia in the early stages of phthisis may be due 
to restlessness owing to worry because of the diagnosis of a dangerous 
disease, and is often removed by emphatically reassuring the patient. 
Indeed, the characteristic attitude of optimism soon prevails and the 
patient is no more disturbed by insomnia. 

In others insomnia is due to excessive cough, or nightsweats, or 
both. In some cases the administration of hypnotic remedies is of 
no avail so long as they are given in safe doses. Especially prone to 
insomnia are patients who suffer from paroxysmal attacks of cough, 
each fit waking them and keeping them awake for one-half to two 
hours. In these cases the administration of codein, morphin, etc., is 
imperative. Profuse nightsweats often act the same way: After 
waking bathed in perspiration, the patient finds it difficult to fall 
asleep again. 

During the advanced stages many patients find it very hard to sleep 
because of the copious secretions in the pulmonary cavities which, 
after a short nap, overflow the bronchi and compel them to rise and 
expel it from the chest. Some with unilateral lesions may be able to 
sleep the greater part of the night in certain positions, and they adapt 
themselves to the conditions. But in others with cavities in both 
lungs, or with sinuses leading from the cavities in different directions, 
the prone posture immediately induces cough. Some have to sleep 
with the face downward if they want to avoid cough, others in the 
semireclining posture, etc. We also meet with cases in which dyspnea 
is the cause of insomnia. While during the early stages of phthisis 
fever may be the cause of insomnia, it is only rarely the case during 
the advanced stages. The average consumptive has adapted his 
organism to the fever and does not mind it very much. Tuberculous 


1 Arch. gén de méd., 1900, 2, 258. 

2 Tt is interesting to mention some of the notable men and women who were tuber- 
culous. Among them may be mentioned: Rousseau, Milton, Kant, Locke, Hawthorne, 
Keats, Shelley, Emerson, Washington Irving, Chopin, Laennec, Spinoza, Hurrell Froude, 
Sterne, Thoreau, Charlotte Bronté, Ruskin, Robert Pollok, Kingsley, Channing, Michael 
Bruce, Béranger, Thomas Hood, James Ryder Randal, Lanier, Scott, Elizabeth Barrett 
Browning, Bichat, Moliére, Rachel, Calvin, Bastien-Lepage, Robert Louis Stevenson, 
Watteau, Jane Austen, Francis Beaumont, David Gray, Richard Lovelace, Georges 
de Guérin, Voltaire, Amiel, Paganini, von Weber, Nevins, Marie Bashkirtseff, John 
Addington Symonds, George Ripley, Paul Laurence Dunbar, Westcott, Blackmore, 
Joseph Rodman Drake, Kirke White, Stephen Crane, Adelaide Anne Procter, N. P. 
Willis, Henry Timrod, H. C. Bunner, John Sterling, R. Koch, Count Leo Tolstoi, Maxim 
Gorky, and many others. 


298 NERVOUS SYMPTOMS OF PHTHISIS 


patients with high fever are often seen sleeping quite soundly as long 
as the cough, nightsweats, and dyspnea do not disturb them. 

In the terminal stage we often observe abnormal somnolence in 
phthisical patients. For days, at times for weeks, the patient lies in a 
semicomatose condition, careless about his person, and only now 
and then wakes to ask for some nourishment. If not due to excessive 
sedative medication, it may be an indication of meningeal complica- 
tion. But I have had cases in which this abnormal somnolence has 
existed for several days or weeks before death, and the autopsy showed 
no meningeal tuberculosis. Some of these patients have periods when 
they are mildly delirious. 

Influence of Tuberculosis on the Sexual Sphere.— The tuberculous 
toxemia has a profound influence on the sexual organs and their 
functions. In women, menstrual disturbances are not uncommon 
during the course of the disease, and quite often these disturbances 
are noted before the onset of evident symptoms of the disease. In 
young girls the appearance of menstruation may stay the progress of 
the disease, as I have seen in several cases. Probably for this reason 
ancient clinicians thought that amenorrhea was a cause of phthisis. 
Now we know it to be an effect of the disease. Amenorrhea is very 
frequent during the course of phthisis, and other menstrual disturb- 
ances, dysmenorrhea, menorrhagia, metrorrhagia, etc., may be ob- 
served in many cases. But I know a large number of tuberculous 
women in whom the menstrual function remained practically normal 
throughout the course of the disease. 

During the menstrual days, and at times a few days before the 
appearance of the flow, there is often observed an aggravation in the 
pulmonary condition. The fever may rise, the cough increases in 
intensity, rales increase in number and extent, or reappear in places 
where they were noted before but had disappeared and new areas of 
lung tissue are often invaded during this period. Hemoptysis is quite 
frequent during this period and in rare cases it may even replace 
menstruation. Premenstrual fever is occasionally noted, as was already 
stated (see Chapter IX). 

Conception is possible at any stage of the disease, and the pregnancy 
may, and often does, pass through almost normally, the child being of 
average weight but often of low vitality. Reibmeyr believes that 
tuberculous women are more prolific than healthy women—Nature 
attempts to compensate in quantity for inferior quality. Abortion 
and miscarriage are said to occur more often among them than in 
healthy women, but this has not been proved conclusively. It appears 
that during pregnancy the tuberculous process is, as a rule, in abeyance, 
and the patient may even improve. (See Chapter XXX.) 


CHAPTER XIV. 
INSPECTION AND PALPATION. 


The Stigmata of Phthisis.— After the history and symptomatology 
of the patient have been carefully inquired into, the physical exami- 
nation should begin with inspection of the physical make-up of the 
individual. In phthisis not only the chest should be carefully examined 
but also the head, the face, the neck, the abdomen and the extremities. 
The stigmata of this disease are often scattered over various parts of 
the body, and the experienced eye may, at times, find outside of the 
region of the chest certain signs which are highly suggestive of phthisis. 
In some borderland cases these stigmata may be of great assistance 
in formulating an opinion on the diagnosis and prognosis. 

Complexion.—Hippocrates described the habitus phthisicus—the 
“form of the body peculiarly subject to phthisical complaints’’—as 
characterized by a smooth, whitish skin, blue eyes, blond or reddish 
hair, and a phlegmatic temperament. Following this ancient clinician, 
many modern writers on this subject have stated that the external 
appearance of certain persons betrays a strong predisposition to this 
disease. 

Hippocrates’ notion that blond-haired and blue-eyed persons are 
more prone to phthisis has survived to this very day, and Beddoe, 
Landouzy, Delpeuch, Piéry, Woodruff, and many others hold the 
same view. Exact information, however, does not sustain this opinion 
that fair-complexioned people are more prone to tuberculosis. In 
countries with predominant blond populations, like Scandinavia, 
England, Northern Germany, etc., the consumptives are generally 
blonds; while in Italy, Spain, Greece, etc., where the dominant racial 
elements are brunettes, the consumptives are of the same complexion, 
as can be seen on visiting the sanatoriums in these countries. In 
China and Japan there are no blonds, yet tuberculosis is not lacking. 
Evidently infection, the length of time a people has been exposed to 
the tubercle bacilli and, above all, social and economic conditions are 
of greater importance in determining the rates of morbidity and mor- 
tality than race or color. 

Facies.—The confirmed consumptive presents a characteristic, in 
fact, an unmistakable appearance, which betrays his disease not only 
to the experienced physician, but also to the laity, and he can often 
be picked out from a group of healthy people with comparative ease 
and certainty. The emaciated body, the pallor of the face with the 
hectic flush on the cheeks, the round shoulders, and the bodily decrepi- 





300 INSPECTION AND PALPATION 


tude, may be seen in other wasting diseases; but the facies of the 
consumptive, while possessing all these traits, has other characteristic 
stigmata. In very few other diseases is there to be seen such a pathog- 
nomonic facial expression as in the consumptive. 

The facial muscles are wasted, the cheeks sunken, and the malar 
bones protrude; the lips are pale or livid, often contracted, as if smiling 
or grinning; the hectic flush, which may be unilateral; the thin neck 
appears longer than normal, the sternomastoids are accentuated like 
two tense bands on both sides; the head is bent forward between the 
two round shoulders, and the spine is bent. Because of the wasting, 
the ears appear larger; one may be redder than the other. 

But the most pathognomonic parts of the cast of countenance of 
the consumptive are his eyes. They are deeply set in the sockets, 
which appear larger than normal because of the wasting of the orbicularis 
palpebrarum. We also meet with a widening of the palpebral aperture, 
and a slight protrusion of the eyeball on the affected side as a result 
of irritation of the sympathetic. A narrow palpebral aperture with 
a somewhat deeply set eyeball is a symptom of prolonged irritation 
of the nerve paths, and is met with in cases with adherent apical 
pleura, as was shown by Kuthy. To the same cause has been attrib- 
uted unilateral dilatation, or more rarely, contraction of the pupil 
which may precede the evident onset of active disease. 

The appearance of the eye as a whole is pathognomonic and can 
be more easily recognized than described. It has a characteristic 
brillianey which has been described as transparent, lustrous, bright, 
dimly brilliant; it differs from the brilliancy of the eyes in other fevers 
in the fact that it appears gloomy, dismal, or haunted—its glance can 
always be felt. Some have attempted to explain these characteristics 
as due to the widely dilated pupils, while the pearly-white sclerotics 
are said to be an expression of vasomotor influence on the bulbar 
conjunctiva resulting from pressure on the cervical sympathetics and 
are to be seen mostly in cases of adherent apical pleurisy. 

This facies has been recognized by the laity, and the folk-lore of 
Europe abounds in sayings about the facial expression of the consump- 
tive. Writers of fiction and painters have also considered it “ inter- 
esting,” and have made great use of it in their productions. Many of 
the classical and modern painters have depicted this cast of countenance, 
showing the false euphoria of the smiling, tranquilly bright, yet 
melancholy eyes of the consumptive, which are perhaps best seen in 
Leonardo da Vinci’s La Gioconda—a picture of a phthisical face 
superior to any description that can be given of it. 

I have seen these facies in some patients with latent, or quiescent, 
tuberculosis in whom physical exploration of the chest showed but 
indefinite signs of an active lesion. It appears to be especially marked 
in persons of phthisical stock and in young individuals with glandular 
tuberculosis, those who were infected during childhood, but have more 
or less recovered. 


THE NORMAL CHEST 301 


The Skin.—Other stigmata of phthisis, which may be noted in the 
early stages of the disease, should be mentioned. On the forehead and 
upper parts of the cheeks we may see chloasma phthisicorum, and in 
those who sweat profusely, pityriasis versicolor and tabescentium on 
the anterior and posterior aspects of the chest. In those who suffer 
from dyspnea, we may find clubbed fingers, or deformities of the hands, 
wrists, spine and tarsus, which are the results of pulmonary osteo- 
arthropathy. On the neck, spasm or atrophy of the muscles, which 
will soon be described, may give a clue that a careful examination 
of the chest is indicated. 

Enlarged Glands.—Visibly enlarged glands are quite rare in adults, 
though I have seen cases in which they went on to suppuration. But 
palpable glands on the neck are very frequent—in at least 50 per 
cent of my cases. In children, enlarged glands are very frequent, 
but they are not always an indication of tuberculosis. If enlarged 
cervical glands were pathognomonic of tuberculosis in children, we 
should find very few who live in poverty free from this disease (see 
Chapter XXIV). Of greater importance from the diagnostic stand- 
point is enlargement of the supraclavicular glands, especially when 
found unilaterally. It speaks for tuberculosis of the costal pleura. 

We also very often find enlargement of the thyroid gland in tuber- 
culous subjects, at times in the incipient stage, and mild grades of 
exophthalmos are not uncommon. The reciprocal relation between 
hyperthyroidism and tuberculosis is discussed in Chapter XXX. 

Enlarged Veins on the Chest.—Enlarged veins are often seen on the 
chest, especially in the infraclavicular region over the first and second 
interspaces, and posteriorly opposite the first thoracic spine, and below 
along the line of insertion of the diaphragm. The upper enlarged veins 
are caused by the interference with the emptying of the internal 
mammary and intercostal veins, because of pressure on the vena azygos 
by swollen thoracic glands, and also by the increased expiratory efforts 
while coughing. They are occasionally seen in healthy persons, espe- 
cially in nursing women, and they may be unilateral in patients suffer- 
ing from chronic bronchitis and pulmonary emphysema, as well as 
with endothoracic tumors. According to Lombardi,! the varicosities 
in the neighborhood of the seventh cervical and first thoracic vertebree 
may be seen in 80 to 90 per cent of cases of phthisis, but I see them 
very frequently in persons without any active pulmonary disease. 

It will also be noted in some cases that the nipple is located lower or 
more externally, while in women the mammary gland may be smaller, 
and the nipple may be less pigmented, than on the opposite unaffected 
side. 

The Normal Chest.—Before looking for pathological changes in the 
form and structure of the chest we must have a clear idea as to what 
constitutes a normal thorax, and it must be stated at the outset that 


1 Gior. internaz. di Sci, med., 1913, 35, 751. 


302 INSPECTION AND PALPATION 


a normal, well-formed chest is an ideal which is not encountered more 
often than physical perfection in general. 

The chest in a normal person is symmetrical; the two sides are 
practically alike. Both clavicles run horizontally, are not very promi- 
nent at their external third; only their contour is visible. The supra- 
and infraclavicular fosse are only slightly deepened, and both to the 

same degree. When the arms hang by the sides the scapule lie flat 

on the bate of the chest extending from the second to the seventh ribs; 
in rare instances they are lower, from the third to the eighth ribs. The 
supra- and infraspinous fosse are filled out with muscles. The spinal 
column runs in a straight vertical line, showing a slight convexity back- 
ward at the upper half of its dorsal portion. The ribs run downward 
and forward, are hardly visible in the upper third of the chest because 
they are covered with muscles and subcutaneous fat, while in the lower 
third they are clearly prominent, and the intercostal spaces are per- 
ceptibly indented. Anteriorly the costal arches form almost a right 
angle, between 60 and 80 degrees; the sternum is straight in profile, 
about 16 to 20 em. in length, and Ludovig’s angle, at the junction of 
the manubrium and gladiolus, is hardly visible. In some persons enjoy- 
ing perfect health, akon Ss groove, denoting the insertion of the 
diaphragm, runs horizontally, commencing at the lower end of the 
sternum and passing downward to the axillary line. The two shoulders 
are of the same height; so are the nipples. The antero-posterior 
diameter is somewhat ‘shorter than the transverse. All the diameters of 
the chest should increase from above downward, giving it the appear- 
ance of a pyramid with its base below. But this pyramidal form is not 
very evident in the average healthy person because of the muscles, 
female breasts, and the clavicles over its apex. During the first year 
of life the transverse diameter is almost as large as the antero-posterior; 
a transverse section appears almost round (Fig. 15). With the growth 
of the child, this infantile form of chest changes, the transverse diam- 
eter Increasing in length, sothat in a childof ten, asection would appear 
elliptical, because of the various projections of muscles, ete. 

The ideal chest, seen perhaps only in the works of great sculptors, 
is, of course, rarely seen in practice because of slight hypertrophy of 
the muscles on the right side in those who work hard, slight shoulder 
droop in those who Have minor forms of scoliosis, etc., all iG which are 
consistent with perfect health of the thoracic viscera. 

While the ideal chest is only rarely seen in healthy persons, it is 
never seen in tuberculous patients. In the latter, going hand-in-hand 
with the progress of the disease, the form and shape of the thorax 
change as a result of certain changes in the respiratory muscles, and in 
many cases we find on inspection and palpation conditions which are 
characteristic of the phthisical chest. 

The So-called Phthisical Chest.—Beginning with Hippocrates, Galen, 
and Aretaeus, physicians and the laity have for centuries associated 
certain forms of abnormal appearance of the chest with tuberculosis, or 


THE SO-CALLED PHTHISICAL CHEST 303 


with a predisposition to this disease. It has thus come about that 
nearly all deformities of the chest excite suspicion of active or latent 
tuberculosis. The fact is that there is no form of the chest which is 
pathognomonic of pulmonary tuberculosis, though there are certain 
changes in its appearance which point to this disease. 

The flat chest, the paralytic chest, and the pterygoid or alar chest are 
very frequently seen in youthful tuberculous subjects, though they are 
also often seen in individuals who pass through life without developing 
tuberculous disease of the intrathoracic viscera. In the flat, or par- 
alytic, chest the ribs run steeply downward toward the sides, and the 
result is that the anterior portions of the ribs and cartilages appear flat 





Fie. 54.—The “‘phthisical’”’ or flat chest. Habitus phthisicus. 


instead of convex; in other words, the chest appears as if it were in a 
state of extreme expiration. It is very long, narrow, and flat, the inter- 
costal spaces appear narrower but excessively deepened, especially over 
the lower half of the chest. The antero-posterior as well as the trans- 
verse diameters are shorter than normal, the scapule move to the 
sides, and appear winged as a result of the reduction in the space 
available for them on the back of the chest, and also because of atrophy 
and loss of tonicity of the muscles, especially the serrati. The clavicles 
are very prominent, and the fosse above and below these bones are 
strikingly deepened. As was already stated, Freund insists that in this 
sort of thorax the first costal cartilage is shorter than normal, only 3 cm, 


304 INSPECTION AND PALPATION 


long in men and 2.2 cm. in women as against 3.8 and 3.1 cm. respectively 
in normal persons. his shortening, together with ossification of the 
first cartilage, produces a narrowing of the upper thoracic aperture, 
which is said to be a strong predisposing factor to tuberculous disease 
of the lung apex. When other costal cartilages are also ossified, as is 
often the case in phthisis, the elasticity of the bony framework of the 
thorax is impaired and expiration is interfered with. The shoulders 





Fig. 55.—The ‘‘phthisical chest.’”? Full-blooded Indian. (Musser.) 


are usually sloping on both sides, the attachment of the ribs to the 
sternum is at an acute angle, and they run obliquely downward to the 
sides. The inferior costal margins reach down very low, almost to 
the crest of the illum in some cases, the subcostal angle is very acute, 
reaching 25 degrees in some instances, and the angle of Louis appears 
as a strongly marked ridge. The spinal column usually shows a strong 
kyphotic bend of the dorsal portion without compensating lordosis of 


TECHNIC OF INSPECTION AND PALPATION OF THE CHEST 305 


the lumbar part. Because of the lack of subcutaneous fat, and the 
atrophy of the muscles of respiration, some have called this form of 
chest the asthenic. 

There are to be distinguished two forms of this chest, the congenital 
and the acquired. The congenital may be hereditary, when occurring 
in newborn infants from tuberculous parents, but this is rare. It is 
mostly seen in infants of poor constitution, in the rachitic and under- 
nourished. In adults it is seen mainly in individuals whose muscular 
system is poorly developed, thus presenting evidences of the asthenic 
constitution. The intercostal muscles being weak, inspiratory efforts 
are feeble and do not expand the chest properly. It is thus said to be 
an expiratory chest. Practically, it will be noted that in most cases 
only the upper part of the chest does not breathe properly. 

It is not wise to condemn a person with this type of chest to tuber- 
culosis, or even to see in it a strong tendency to this disease when no 
constitutional symptoms are found. Many, or most, persons with the 
asthenic constitution never develop tuberculosis. There seems to be 
available evidence to the effect that this asthenic chest is the result 
of ancient tuberculous infection, especially during childhood, affecting 
the intrathoracic glands, and that the lesions have healed. Elsewhere 
in this book we show that these tuberculous infections have a certain 
immunizing effect against the development of active phthisis in the 
adult. 

With the acquired form of the flat chest things are different. Persons 
with this type of chest have either active, or quiescent tuberculous 
lesions in the lungs. In most cases it will be noted that the symmetry 
of the chest is more or less disturbed; the muscles of respiration, the 
trapezu, the pectorales, the rhomboidei, the scaleni, etc., are unduly 
contracted when the tuberculous lesions are early, or atrophied on one 
side of the chest with advanced or healed lesions. The diaphragm, the 
only muscle to act during respiration, is often immobile on one side 
owing to pleural adhesions and destruction of the pulmonary paren- 
chyma. One scapula is more winged than the other, or nearer the 
middle line. One shoulder is lower than its mate, and there are seen 
retractions of the chest wall on the side which is most affected. These 
changes are discussed further on in this chapter. 

Technic of Inspection and Palpation of the Chest.—In addition to 
the light, warm room and stripping the patient to the waist, which 
are self-evident requirements, the patient is to be seated on a round 
stool, directly facing the window or the source of artificial light. He 
is permitted to assume his natural posture without urging him to sit 
straight up, hold his head in the middle line, etc., so that we may 
note any faulty position of the head, neck, spine and chest. Careful 
attention is to be paid to the position of the head, the shoulders, the 
clavicles, the ribs and the scapule during rest, during moderate, and 
forced breathing. 

Above all, we are looking for evidences of asymmetry in structure, 

20 


306 INSPECTION AND PALPATION 


form, and mobility, when the two sides of the chest are compared. Motion 
can be ascertained by inspection, carefully noting from a distance the 
tips of the acromion processes, as well as the elevation of the ribs 
during inspiration, the position of the scapule during both phases of 
the respiratory act, and also the lateral expansion of the lower parts 
of the thorax. Flattening, excavations, and undue prominence of the 





Via. 56.—Emphysema with enlargement of the chest; the antero-posterior diameter is 
much increased. (Musser.) 


respiratory muscles are to be especially looked for. The supraspinous 
and supraclavicular fosse are compared, and no deviation from the 
normal should be overlooked. Spinal deformity, if present, must 
be given attention, for it may be the result of an intrathoracic lesion; 
because it may have an immense influence on the interpretation 
of the results obtained by percussion and auscultation, and also on 
the roentgenogram. ‘ 


TECHNIC OF INSPECTION AND PALPATION OF THE CHEST 307 


The motion of the anterior aspect of the thorax is well studied while 
standing behind the patient and looking over his head, watching the 
ribs and clavicles as they rise and descend during inspiration and 
expiration, and noting any retardation or limitation of motion on one 
side as compared with the other. It is, however, best to ascertain 
this by palpation, placing the hands on each side of the patient’s 
neck, the thumbs meeting behind at the spine and fingers reaching 
down over the clavicles (Fig. 57), and for the lower parts by placing 
the hands over the lateral aspects of the chest. In this manner slight 
differences can be detected more easily than by inspection. Special 
attention is to be paid to lagging—one side of the chest is delayed in 





Fig. 57.—Testing mobility of the chest. 


movement and, in more advanced cases, expansion is limited. At 
times we meet with both lagging and limitation of motion in various 
parts of the chest and we may conclude that the former is an indica- 
tion of a recent lesion, while the latter is caused by an old, probably 
pleuritic lesion. 

Spasm and degeneration of muscles of the neck and chest are best 
ascertained by Pottenger’s method of “light touch palpation.” Press- 
ing the tips of the fingers over the muscles under consideration and 
moving the hand sidewise, carefully noting the degree of resistance, 
will show this condition. While doing this the fingers should not be 

allowed to slip on the skin, because it is the condition of the muscles, 


308 INSPECTION AND PALPATION 


and not of the skin, that we wish to ascertain. Over acute lesions it 
is found that the muscles give to the palpating fingers a distinct feeling 
of increased resistance, that they are firmer and fuller than normal, 
while over advanced lesions there is a flabby, doughy feeling, and the 
bundles can be easily separated owing to atrophy and degeneration. 

Significance of Lagging.—In the very incipiency of a pulmonary 
lesion we often note that the affected side of the chest begins to expand, 
and the shoulder to move upward, later than the opposite healthy side 
of the chest, and finally does not attain the same amount of expansion. 
In far-advanced cases and in those with pleural adhesions and effusions, 
pneumothorax and intrathoracic tumors, there may even be absolute 
immobility of the affected side. It is best ascertained by letting the 
patient first breathe normally and then asking him to take a few deep 
inspirations. 

Lagging of the upper part of one side of the chest is an indication 
of a lesion in that apex, provided an acute or chronic non-tuberculous 
inflammatory process of the lung and pleura is excluded. When the 
motions of both sides are equal, but there are sure signs indicative of 
tuberculosis, we may conclude that there is a bilateral lesion. With an 
old quiescent lesion in one side and a new and active lesion in the other, 
the lagging is more pronounced in the newly affected side. I often find 
difficulties in clearing up by inspection and palpation old bilateral 
lesions in which both sides show limited motion. In these, percussion 
and auscultation give more reliable information. But in incipient 
unilateral cases inspection is of immense value. 

Thoracic Asymmetry.—Looking at the phthisical chest anteriorly, 
in cases in which the disease has already made some inroads, we find 
some undue prominence, even arching of the clavicle and more or less 
deep excavation jn the supra- and infraclavicular fossze, more marked, 
or exclusively, on the affected side. The angle of Louis at the junc- 
tion of the manubrium and the gladiolus is more pronounced than in 
the average healthy chest. Posteriorly, we find kyphosis in many 
cases, the scapule are prominent, winged, and even dislocated, nearer 
the spine on the affected side. The intercostal spaces are narrow, but 
deeply indented and, in extreme cases, thefree margins of the costal carti- 
lages nearly meet in the middle line. In addition to these changes we 
meet with distortions of various parts of the chest, especially the upper 
half—flattening and retractions of various degrees anteriorly and 
posteriorly. Depression of the acromial end of the clavicle on the 
affected side may be already noted in the very early stages of the 
disease. Kuthy! found it in 82 per cent of his incipient cases. 

Inspiratory Retractions.—In patients with far advanced lung lesions 
localized inspiratory retractions may be seen on the chest wall. In 
some instances in which large cavities exist in the upper lobe we may 
note during each inspiration a cup-shaped depression of the intercostal 


1 Sixth Internat. Congr. Tubere., 1908, 1, 1215. 


SPASM AND DEGENERATION OF THE THORACIC MUSCLES 309 


space covering the cavity, usually the second, third or fourth interspace. 
In extensive left-sided lesions pulsation of the displaced heart may be 
visible owing to retraction of the lung and pleural adhesions. When 
there is great difficulty in the entry of air into the alveoli, as is the case 
in acute pulmonary miliary tuberculosis, and pulmonary edema, the 
lower margins of the chest sink in quite deeply during each effort at 
inspiration. This is especially to be observed in children and in 
young adults in whom the chest wall is elastic and yielding. In 
emphysematous individuals, and in patients with tuberculous lesions 
in the upper lobes, but in whom the lower lobes are vicariously emphy- 
sematous, there may be seen inspiratory retractions of the lower margins 
of the chest, because the diaphragm does not move properly and the 
lungs do not fill fully with each inspiration. 


Scalenus post.7.. 
Scalenus med... 
Scalenus ant... ’ 
- fff, 
Trapezius 7.. Mi | 


AMI h 
il | 


WN 


xs 





SN 
SSS 


f 


Fig. 58.—Muscles of the neck which are either spasmodically contracted or atrophied 
in pulmonary tuberculosis. 


Localized inspiratory retractions are excellent signs of airless tissue 
beneath the retracted area. Whether the airless tissue is tuberculous, 
pnheumonic, or atelectatic in origin, or due to pleural adhesions, should 
be made out by a study of the concomitant symptoms and signs. 
Retractions are not to be confused with immobility of a part of the 
chest wall which may be due to pleural adhesions, pain in the chest, 
disease of the muscles, pleural effusions, intrathoracic tumors, etc. 

Spasm and Degeneration of the Thoracic Muscles.—Any, or most, of 
these changes in the contour of the chest may be noted in cases of 
non-tuberculous affections of the thoracic viscera, and also in patients 
who had tuberculous lesions which have healed, the patient being 
in excellent health. Pottenger, in his epoch-making studies of the 
tuberculous chest, has given us certain clues as to the means of differ- 
entiating these conditions. It appears that intrathoracic conditions 


310 INSPECTION AND PALPATION 


have a great influence on the muscles of respiration, a fact which 
has been known for a long time, but was rationally interpreted and 
made available for diagnosis by Pottenger. 

Whenever the lung or pleura is acutely inflamed, the thoracic 
muscles over the seat of the lesion are in a state of spasmodic contrac- 
tion, like the abdominal muscles in a case of appendicitis. Depending 
on the acuteness of the inflammatory process in the pulmonary paren- 
chyma or pleura, the muscles of the neck and chest show this contrac- 
tion in various degrees. As in other visceral inflammations, this is an 
involuntary reflex protective spasm. 

Inspection and palpation reveal this condition very clearly in the 
vast majority of cases. Muscles in spasm are larger and firmer in 
appearance as well as to touch, giving a distinct feeling of increased 
tension. Often the more tendinous parts of muscles feel like distinct 
cords, while the more fleshy parts are larger and firmer to the touch 
than normal muscles on the opposite unaffected side. 

After the inflammatory process in the lung and pleura has lasted 
for some time, and passes into a chronic stage, the muscles degen- 
erate; they waste and become flabby. To the palpating finger they 
feel doughy, their normal tone and elasticity are gone, and their bundles 
are easily separated. It is important to note that, coincident with 
this change in the muscles, there is always seen atrophy of the skin 
and disappearance of the subcutaneous tissue. Some of these changes 
are evident to the sight as well as to the touch. 

Pottenger looks upon these muscle changes as due to reflex stimula- 
tion of the motor nerves, the result of continuous irritation caused by 
the impulse from the inflamed lung and pleura. When this irritation 
is kept up very long degeneration and wasting follow, though the 
latter may be due partly to trophic disturbances. But if it is true that 
we can make out by superficial palpation of the dead body internal 
solid structures, as some have maintained, it would indicate that the 
theory of reflex irritation is inadequate. 

Muscular Changes in Incipient Cases.—In incipient cases we often 
find that the sternocleidomastoid, the scaleni, and pectoralis anteriorly, 
and trapezius, levator anguli scapuli, ete., posteriorly, are in a state 
of spasm: They stand out more prominently, are larger and firmer 
to the touch than the same muscles on the opposite, unaffected side. 
I have often seen that as a result of this spasm the supraspinous fossa 
was fuller at first sight. When occupational influences can be excluded, 
it is a good sign of active incipient phthisis. When combined with 
lagging of the same region, or, at the base of the same side, it is 
undoubtedly a sign of a lesion of the lung, provided non-tuberculous 
disease can be excluded. ‘To distinguish these changes in the muscles 
from those resulting from occupational influences, it is to be borne in 
mind that the sternocleidomastoid muscles rarely, if ever, hypertrophy 
or waste from overuse, or disuse, nor does the subcutaneous tissue show 
any changes. 


EFFECTS OF MUSCULAR ATROPHY ON THE THORAX 311 


Muscular Changes in Advanced Disease.—With the advance of 
the disease, the affected muscles, as a result of prolonged spasm, 
begin to atrophy and degenerate. The result is that on inspection 
and palpation even better criteria of the intrathoracic condition may 
be elicited. The degeneration of the skin and subcutaneous tissue 
over the site of the lesion is seen at once; the skin can be lifted up 
with the fingers more easily, and it is felt that it lacks the normal 
elasticity. The sternocleidomastoid, scaleni, pectoralis, trapezius, 
levator anguli scapulee and rhomboidei all look smaller than their mates 
on the unaffected side. They are flabby and doughy to the touch. 

In cases with old circumscribed lesions limited to the upper part 
of the apex we may find the upper half of the pectoralis degenerated 
and flabby, while the lower half is normal. As a result of atrophy of 
the trapezius we find flattening of the supraspinous fossa; in extreme 
cases it appears cupped. In old cases extension of the disease may 
often be ascertained by inspection and palpation. The old lesion on 
one side shows wasting of the skin and muscles, while on the opposite 
side, where tubercles have just formed a new incipient lesion, the 
muscles are in spasm—contracted and prominent. Lagging is more 
pronounced on the newly affected side; it indicates an active lesion 
which hinders motion of the contracted muscles, especially the dia- 
phragm. “When palpation, percussion and auscultation show evi- 
dences of a lesion and there are changes in the mobility of the suspected 
side and no spasm of the muscles over the apex but, on the contrary, 
the tone of the overlying muscles has decreased, and there are evidences 
of atrophy of the subcutaneous tissue combined with clinical symp- 
toms of tuberculosis, we are justified in concluding that we deal with 
an old, inactive, or healed process.” (Pottenger.) 

In many cases we may find the regional muscles more or less atro- 
phied from disuse, especially when compared with the opposite side, 
where they are enlarged, firm, and prominent because of excessive 
occupational hypertrophy. This is best differentiated by bearing in 
mind that in muscular atrophy due to disuse, the subcutaneous tissue 
is normal, while when due to a pulmonary lesion it is atrophied. 

Effects of Muscular Atrophy on the Thorax.—Lagging, which was 
formerly attributed to lack of expansion of the affected lung or 
pleural adhesions, is better explained by the tonic contraction of the 
scaleni and sternocleidomastoid on the affected side, which raise and 
fix the sternum, and immobilize to a certain extent the first and second 
ribs, thus limiting the respiratory motion of the affected side. Round 
shoulders, which were formerly attributed to weakness of the pos- 
terior muscles which hold the spine erect, are more rationally explained 
by Pottenger as due in a great measure to shortening of the anterior 
muscles through spasm and degeneration, together with lessened 
mobility of the thorax. Flattening of the chest, especially over pul- 
monary cavities, which was formerly attributed to atmospheric pres- 
sure forcing the bony thorax inward, in order to occupy space 


312 INSPECTION AND PALPATION 


previously occupied by lung tissue, is explained by Pottenger as due 
to inflammatory disease within the thoracic cavity, and reflex inter- 
ference with the normal motion of the diaphragm, which is known to 
be part and parcel of phthisis from roertgenographic studies. 

Bearing in mind that the vast majority of persons are infected with 
tuberculosis during childhood, but that the pulmonary lesions heal, 
or remain latent, it is understood that the lesions produce muscular 
changes in the manner described above during the time of their activity. 
Thus, we have an explanation for the origin of the phthisical or par- 
alytic thorax. It is a result of an earlier infection which has healed 
or remained latent and quiescent and is not a predisposing cause of 
phthisis. A careful study of children of tuberculous parentage has 
shown that, as a rule, they are born with normal chests, and the 
characteristic deformity only occurs later in life after infection with 
tubercle. 

Vocal Fremitus.—Palpation for the vocal fremitus is of but little 
diagnostic value in any stage of phthisis, excepting in cases where 
pleural effusions are suspected. But it is often absent in thickened 
pleura and intrathoracic neoplasms and thus is not of great assistance 
in our attempts at differentiating the latter from an effusion. Of 
course, it 1s increased over consolidations of lung tissue, and when due 
to tuberculosis, consolidation may thus be elicited by palpation for the 
vocal fremitus. But the consolidation must be extensive, involving 
the greater part of a lung, to be easily discovered by palpation. In 
early lesions the writer’s experience has shown that percussion and 
auscultation elicit definite signs, but the vocal fremitus remains normal 
in most instances. 

Myoidema.—In some cases of tuberculous disease of the lung 
myoidema may be observed—a nodular swelling of a muscle produced 
by tapping it with the finger, or filliping it, which causes a local contrac- 
tion lasting several seconds and disappearing. It should not be 
confused with another kind of muscular contraction induced by per- 
cussion, the fascicular, consisting in a deep furrow along the entire 
length of the muscle; in myoidema merely a nodular swelling is pro- 
duced; hence it has also been called nodular contraction. It was first 
described by the great Irish clinician William Stokes in the Clinical 
Report of Cases in the Medical Wards of the Meath Hospital during 
the Session of 1828 and 1829.1. “Some time ago, on percussing a 
patient (immediate percussion was then practised) who had labored 
under a pectoral affection, with several symptoms indicative of tubercu- 
lar development, we were surprised to observe that after each stroke 
of the ends of the fingers a number of little tumors appeared, answering 
exactly to the number and situation of the points of the fingers where 
they had struck the integuments of the chest. These having continued 


1 Dublin Hospital Reports, vol 5, quoted from Stokes’s Treatise on the Diagnosis and 
Treatment of Diseases of the Chest, New Sydenham Society, p. 429. 


MYOIDEMA 313 


visible for a few moments, subsided; but could be again made to 
appear on repeating the percussion.” 

This sign was practically forgotten until recent years, when several 
authors began to publish papers on a new sign of tuberculosis con- 
sisting in hyperexcitability of the muscles. Verrienti' says that this 
muscular hyperexcitability is a phenomenon which is present in all 
stages of phthisis, is most marked on the side with the most active 
lesion, not necessarily where the changes are most extensive. All the 
muscles of the body may thus react to percussion, but those of the 
thorax, especially the supraspinatus, pectoralis major, and the trape- 
zius, show it in a most pronounced manner. It is attributed to super- 
saturation of the body with the toxins of tuberculosis, especially the 
muscles, the smooth as well as the striated. Flushing of the cheeks, 
turgescence of the veins, diarrhea without tuberculous ulcerations 
of the intestines, irritability of the heart muscle, etc., which are 
observed during the course of phthisis, are all due to this muscular 
hyperexcitability. Halbron, Pradal, Sainton,? F. Levy, Theodorescu,’ 
and many others, are inclined to attribute great diagnostic and prog- 
nostic significance to this myotonic reaction. They point out that it is 
absent in chronic bronchitis and in pulmonary emphysema, and when 
these conditions are complicated by tuberculosis, rendering it difficult 
to localize the lesion, the side in which the tuberculous process is 
located may be discovered by detecting myoidema. 

But Stokes already, in 1828, pointed out that myoidema is not alto- 
gether pathognomonic of phthisis. He said: “There is nothing in this 
muscular irritability peculiar to phthisis, but that it is commonly 
connected with irritation of the lung, or pleura, there can be no doubt; 
and in this way, like other signs of irritation, it becomes available in 
the diagnosis of phthisis. It is always more evident in the earlier 
periods; thus in incipient phthisis it occurs over the primary seat of 
irritation, while in the confirmed and chronic cases we may often find 
it absent over the diseased lung, and strikingly marked on the side last 
and least engaged.”’ More recently 5S. West* investigated this sign 
and found it present in tuberculous patients, and also in many others, 
healthy, as well as sick with various diseases involving emaciation, or 
absence of subcutaneous fat, which is one important factor in its 
production. In some people it is probably physiological. Many 
recent writers have found it in numerous morbid conditions of toxemia 
and nervous fatigue, such as plumbism, alcoholism, cancer, various 
infections, notably typhoid fever, lethargic encephalitis, acute articular 
rheumatism, nephritis and uremia, Addison’s disease, ete. 

Myoidema can therefore not be considered a sign pathognomonic 
of tuberculous disease of the lung or pleura. 


1 Riforma Med., 1919, 35, 571. 

2 Bull. et mém. Soc. méd. d. hép. de Paris, 1919, 48, 980. 

3 Tbid., p. 973. 

4 Diseases of the Organs of Respiration, London, 1909, p. 510. 


CHAPTER XV. 
PERCUSSION OF THE CHEST IN PHTHISIS. 


Waite the value of percussion in the diagnosis of conditions in the 
advanced stages of phthisis, and its complications, is not questioned, 
it has been very seriously debated whether it can give dependable 
information in the early, or incipient, stage. Many authorities, not- 
ably of the French school, like Grancher, Bezancon, Barbier, Piéry; 
and also 8S. West, Bonney, Lawrason Brown, Henry Sewall and others 
maintain that small tuberculous foci in the lung in incipient phthisis 
can be recognized solely through recourse to auscultation, and that 
when dulness is elicited on percussion, we may be confident that we 
are dealing with extensive infiltration—a more or less advanced stage 
of the disease. On the other hand, Aufrecht, Kroénig, Goldscheider, 
William Ewart, Lees, Riviere, and many others, maintain that if we 
are to detect incipient lesions in phthisis, we must resort to percussion, 
and it is only when the process has advanced that definite auscultatory 
signs are elicited. 

Aims of Percussion.—It seems that these differences of opinion 
are mainly due to a misapprehension as to the aims of percussion. 
Those who expect to make a diagnosis relying solely on percussion 
findings will be sadly disappointed, just as they will fail in attempt- 
ing to draw final conclusions from any other single symptom or sign. 
Percussion only gives information about the density, or the air content, 
of the lung at the point examined. Whether an airless area thus detected 
is due to a tuberculous infiltration, or to one of the numerous other 
factors that may consolidate large or small areas of lung tissue, must 
be determined by a study of all the concomitant symptoms and signs. 
On the other hand, given constitutional symptoms of phthisis such 
as cough, fever, anorexia, etc., signs of a limited infiltration, or of a 
circumscribed area of airless lung tissue, elicited on percussion, may 
enable us to localize the process and complete the diagnosis in the 
absence of auscultatory signs. 

We must bear in mind that phthisis does not begin as a catarrh of 
the small bronchi, as some believe, but as an infiltration, transforming 
the normal porous, air-containing, and resonant lung into solid non- 
resonant tissue. At this stage the alveoli are filled with exudate, or 
the interstitial tissues contract and compress the alveoli, finally 
obliterating them altogether. Inasmuch as altered breath sounds and 
rales can only be found in the pulmonary apices when edema and 
secretions interfere with the entry or exit of the air current while 
passing through the air vesicles and bronchioles, it is clear that auscul- 


AIMS OF PERCUSSION 315 


tation may not give any information at a very early stage. So long 
as the infiltration remains beneath the mucous membrane of the 
bronchi, the entrance of air into the alveoli of the affected area is not 
interfered with very much, while in the rest of the lung it is freely 
circulating. Auscultation may not reveal such a lesion which is 
surrounded by healthy lung tissue working vicariously and sucking 
in more air. 

It is only when the caseous material of the infiltrate softens and 
breaks through the wall of a bronchus, thus permitting the entrance 





Fre. 59.—Outlines of viscera. The margins of the lobes of the lungs are shown 
(interrupted line ------ ); solid black line, heart, liver, and spleen; stomach shaded. 
(After His-Spalteholtz, Luschka, and Musser.) 


of air into the diseased focus proper, that rales can be heard on auscul- 
tation. At that time tubercle bacilli make their appearance in the 
sputum. When we have rales we may be sure that we are dealing 
with a more or less advanced stage of the disease—caseation and 
softening have already taken place. : 

When the tuberculous process was not located originally in the bron- 
chioles, but in the peribronchial tissues, it is again evident that the air 
circulating in the bronchial tree cannot reach the tubercle at all, and 
the auscultatory signs will necessarily be negative. At most, feeble, 


316 PERCUSSION OF THE CHEST IN PHTHISIS 


or the absence of breath sounds over a limited area may be the first sign 
elicited. 

Technic of Percussion.— Percussion has been neglected by many 
because it has not given them the information they sought; at times 
it even misinformed them. The reason is almost invariably faulty 
technic. Before giving details as to percussion findings in early 
phthisis, we must speak about the proper technic to be followed in 
apical percussion. 





Fig. 60.—Outlines of viscera. The margins of the lobes of the lungs are shown 
(interrupted line ------ ); solid black line, heart, liver, and spleen. (After His-Spalte- 
holtz, Luschka, and Musser.) 


The first and most important point in percussion is a light stroke with 
the finger. Heavy blows with two or three fingers are worse than useless. 
Because of the elasticity of the thoracic walls, a great part of the per- 
cussion stroke is always dissipated along the muscular and bony 
parietes, and when we strike a heavy blow most of the force is con- 
ducted laterally by the ribs and intercostal muscles, which are set into 
strong vibration, acting as large pleximeters, and resonance from the 
entire lung beneath is elicited. Small areas of airless tissue are thus 
overlooked. With a light stroke the force is not conducted along the 


TECHNIC OF PERCUSSION 317 


parietes, but penetrates sagitally into the lung, affording information 
about its condition immediately beneath the point examined. 





Fia. 61 Fig. 62 
Fras. 61 and 62.—Margins of the lungs and of individual lobes, dotted line (- - --- - WP 
limits of pleural sacs, interrupted line (------ ); liver and spleen, solid black line; 


diaphragm, starred line (******): stomach (portion not covered by lung) shaded. 
(After Luschka and Musser.) 


With light percussion in which the stroke is gentle and soft, hardly 
audible at any distance, we can always localize areas of superficial 


318 PERCUSSION OF THE CHEST IN PHTHISIS 


dulness. Deep-seated, airless areas cannot be detected by heavy per- 
cussion, as is evident from the fact that we cannot map out the heart 
from behind, and in obese and edematous persons it is quite difficult, 
often impossible, to define the boundary between the liver and the 
lung. Strong blows do not reach much deeper into the pulmonary 
tissue proper than light strokes. To be sure, they set up stronger 
vibrations, but mainly in a lateral direction, and for this reason the 
penetrating power of the heavy blow may be even less than that of 
the light stroke. 

Gentle percussion often brings out small areas of dulness which dis- 
appear with an increase in the force of the blow because larger areas 
have been set into vibration. This point is utilized for diagnostic 
purposes: If, on increasing the force of the blow, the dulness remains, 
we may be sure that we are dealing with extensive areas of airless 
tissue. 

The Pleximeter Finger.— Light percussion is best accomplished when 
the movement of the percussing finger is exerted only from the meta- 
carpophalangeal joint. The note elicited should be only a faint sound 
which can be heard when listening attentively. Of course, perfect 
silence must be maintained in the room. When reaching an airless 
area, the contrast between the resonance evoked in the air-containing 
space and the deadness over the dull area is striking. The contrast 
between something and nothing is easier of appreciation than the 
difference between one thing and another which differs but slightly 
from it. Over resonant areas we evoke a note, while over dull areas 
no note is brought out at all. 

Strong pressure of the pleximeter finger on the chest wall dissipates 
the advantages of light percussion by bringing the intercostal muscles 
into tension, making them large pleximeters, which elicits resonance 
of the neighboring air-containing lung, and small areas of dulness can 
thus not be delineated. Very light contact of the pleximeter finger 
with the chest wall is therefore important; in delicate percussion, the 
mere weight of the finger is sufficient. 

Bearing in mind that, as a rule, tuberculous lesions spread from 
above downward, and that the line between the healthy and infiltrated 
tissue usually runs horizontally, we must percuss from above down- 
ward, or the reverse, in vertical zones. The pleximeter finger should 
be placed parallel with the ribs (Fig. 63) and not perpendicular to them, 
as is often done. It is obvious that when the pleximeter finger is placed 
vertically on the chest we obtain mixed resonance, because the stroke 
brings both healthy and diseased lung into vibration in cases of limited 
lesions. Only intercostal spaces should be percussed because percussion 
of the ribs, which in themselves are to be considered as long plex- 
imeters, brings out resonance due to vibrations of large areas of lung 
tissue which lie laterally, and not ‘only from beneath the spot which 
we intend to strike at the given moment. 

The usual way of beginning percussion at the top of the chest and 


THE PLEXIMETER FINGER 319 


going gradually downward to the base has many disadvantages. It 
is much better to percuss from below upward. N. Kk. Wood! sum- 
marizes the reasons for this procedure as follows: “It is much easier 
for the ear to pick up a higher note from a lower than it is to do the 
reverse; it requires a much lighter stroke to bring out the normal 
note than the pathological; it is the rational plan to work from the 
normal as a standard toward the pathological. The reverse leads to 
faulty standards. The apices, as is well known, are most frequently 
affected and more rarely give a normal note. To start at the apex, 
therefore, is usually to commence with a pathological note. This 
prejudices the further examination. With downward percussion, the 






\ | ae \ 
ee ee f 
ne | gh ors 
= | oe , 
EN J 
Fic. 63.—Percussion of the right apex. 


higher note merges into the lower too imperceptibly to do accurate 
work. Thisissofortworeasons: (1) the mind becomes prejudiced in 
favor of a pathological note and consequently does not attempt to 
make fine distinctions, (2) a heavier stroke is required for the patho- 
logical note, and when the more resonant is reached the percussion is 
continued too heavily to detect what should be readily appreciated 
differences in the force of stroke necessary to bring out a good note. 
In this way the examiner deprives himself of a very important guide 
to collect accurate data.” 


1 Jour. Am. Med. Assn., 1914, 63, 1378. 


320 PERCUSSION OF THE CHEST IN PHTHISIS 


The Hooked-finger Pleximeter.—In incipient phthisis we aim at 
localizing the smallest possible area of dulness, and at times the plex- 
imeter finger is too large for the purpose. Plesch! has suggested that the 
pleximeter finger be flexed at the second phalanx to a right angle; the 
pulp only is applied to the chest and the distal end of the first phalanx 
is percussed (Fig. 64). This maneuver also enables the delimitation 
of the boundaries of the apex, or the determination of the condition of 
the apex behind the heads of the sternocleidomastoid, which is often 
of great importance. 

Position of the Patient.— The patient should sit on a revolving stool, 
or better stand up with his head in the middle line, arms hanging by 
the side in a relaxed condition (Fig. 63). Contraction of any of the 
muscles of the chest on one side may greatly interfere with the results. 
When the back is percussed the patient is asked to fold his arms each 
on the opposite shoulder with a view to removing the scapule as far 
outward as possible. With these bones in the normal position the 





Fie. 64.—Hooked-finger percussion. 


greater part of the lung in the supraspinous fosse is beneath the bony 
thorax, and the apex is partly covered by the shoulder-blades. To 
hammer away in the supraspinous fossee, as we often see done, is a 
waste of time and energy, because percussion there strikes bone and 
thick muscles, and the waves hardly, if at all, penetrate into the lung. 
But with folded arms, each over the opposite shoulder, or the patient 
embracing the back of a chair, the shoulder-blades are moved far 
away from the median line of the body, thus exposing the lung covered 
by comparatively thin parietes. 

When it is desired to bring out the finer shades of resonance or, in 
doubtful cases, it is advisable to have the patient lying down on an 
upholstered couch or an examining table. Placing the patient with his 
back near a wall or door may help in bringing out points which might 
otherwise escape attention. 

Comparative Percussion.—When percussing, we compare symme- 
trically corresponding areas on both sides of the chest and percuss 


1 Miinchen. med. Wehnschr., 1902, 49, 620. 


COMPARATIVE PERCUSSION 321 


with equal force while striking each side. This is especially important 
because there is no standard resonance for a healthy chest; every 
individual has his own resonance which depends on many factors, 
mainly the vibration of the chest walls and the contents of the thoracic 
cavity, which are inconstant values. But in the normal chest the reso- 
nance, in all its properties such as duration, intensity, quality 
and pitch, are practically the same on both sides. 

In incipient cases there are “seats of election’—points where 
dulness is most likely to be encountered if there is an apical lesion. 
Anteriorly, it is mostly under the inner third of the clavicle, and 
posteriorly at the inner margin of the upper half of the scapula. 





Fie. 65.—Percussion of the left apex posteriorly. 


A small area of defective resonance can often be discovered by 
immediate percussion directly over the clavicle, comparing one side 
with the other. Immediately above and below the clavicle mediate 
percussion will bring it out, if it is present. If, on light percussion, 
impairment of resonance is discovered, the force of the blow is dimin- 
ished to a minimum, thus delimiting the affected area, and we can again 
percuss the same spot, gradually increasing the force of the blow, 
always having in mind the thickness of the integuments, with a view 
to ascertaining the degree of dulness. If the dulness disappears with 
a heavy stroke, the lesion is of slight extent and superficial, or there 

21 


322 PERCUSSION OF THE CHEST IN PHTHISIS 


may be a thickened pleura; but if it persists, we may feel confident 
that we are dealing with an extensive area of airless tissue. 

Posteriorly, we look for dulness over the apices of the upper and 
lower lobes of the lung. The former is located in the supraspinous 
fossa near the spine and reaches the first thoracic spine; the latter 
is lower in the right side, reaches the fourth thoracic spine and higher 
in the left side at the third thoracic spine (Fig. 60). If impairment 
of resonance is present in incipient cases, it will be found at one of 
these four points. 

While doing comparative percussion of apices it is imperative to 
remember that, in the majority of healthy persons, the resonance over 





Fic. 66.—Hooked-finger percussion of the apex. 


the right apex above the third rib is somewhat defective; the note is 
shorter and of higher pitch. This has been attributed to various 
causes. Investigations of George Fetterolf and George W. Norris! 
have shown that it is due to the anterior position of the large vessels 
in relation to the right apex, as compared with the left; to the conse- 
quent encroachment upon, and reduction in size of, the right apex 
and to the contact of the inner surface of the right apex with the 
resonating trachea, while the left is in contact with non-resonating 
solid tissue. In right-sided lesions, when the signs are inconclusive, 
topographical percussion is therefore best. 


1 Am. Jour. Med. Sci., 1912, 143, 637. 


TYMPANITIC RESONANCE IN INCIPIENT LESIONS 328 


Tympanitic Resonance in Incipient Lesions.—In the early stages 
the absence of distinct dulness in any part of the thorax is not always 
an indication of the absence of tuberculous infiltration. Impairment 
of resonance can only be brought out when the focus is at least one 
inch in diameter, although some, like Flint and Oestreich, are said to 
have detected smaller foci. But small disseminated tubercles, before 
they become confluent, may alter the resonance in an altogether 
different direction. Causing relaxation or hyperfunction of the sur- 
rounding lung tissue, they impart a tympanitic note on percussion. 
This tympany is of great importance in the diagnosis of incipient 
lesions, and is usually the cause why two competent observers will at 
times detect the lesion on different sides of the chest. 





Fria. 67.—Percussion of the axilla. 


Everyone who has had the opportunity and inclination to watch 
incipient tuberculous lesions has met with cases in which the first sign 
obtained on percussion is localized tympany, which subsequently 
changes into dulness with a tympanitic overnote, and finally becomes 
dull. Tympany in one supraspinous fossa, when accompanied by 
suspicious symptoms, is to be taken seriously; it may be the sole 
indication of small disseminated tubercles. 

Absence of percussion signs, on the other hand, does not exclude 
incipient phthisis, because the lesion may be located deeply, subapi- 
cally, or centrally, or it may be altogether a more malignant process— 


324 PERCUSSION OF THE CHEST IN PHTHISIS 


miliary, or disseminated, tubercles all over the lungs which have not 
yet become confluent. In the same manner, extensive tympany over 
one lobe, or one lung, with fever, cough, etc., may be an indication of 
extensive tuberculization of the affected part. The outlook is not so 
good as when the tubercles are localized in a limited area. 

Respiratory Percussion.—In doubtful cases it is advisable to study 
the changes in the resonance during extreme and held inspiration and 
expiration, as was suggested by J. M. Da Costa! half a century ago. 
He showed that “at the apices, and especially in the infraclavicular 
region, in the supraspinous fosse, and on a line toward the spine, a 





Fic. 68.—Lung margins according to Goldscheider. 


full-held inspiration increases the resonance, makes the sound fuller 
and raises the pitch; and where, as is so common, the left side has 
normally a higher pitch, this disparity is preserved.” A held and 
complete expiration will greatly lessen the resonance and lower the 
pitch at the apices. “In the held inspiration we obtain a greater mass 
of tone; in held expiration, the reverse.” This change of resonance 
was found by Da Costa to remain unaffected in bronchitis; but in 
phthisis, even in the earlier stages, the affected area shows the reverse 
—a long-held inspiration gives a duller note than that observed on 
the healthy side. 


1 Am. Jour. Med. Sci., 1875, 70, 17. 


TOPOGRAPHICAL PERCUSSION OF PULMONARY APICES 325 


This change of note during held inspiration and expiration is brought 
out very clearly by light percussion and is of great value in doubtful 
cases. When the infiltration increases in extent, involving the larger 
part of the apical parenchyma, the dulness on percussion is no longer 
modified by the forced and held expiration and inspiration. Hence we 
have in this method a very good test as to the extent of involvement 
in the tuberculous process. Aufrecht' confirmed these findings. 

Topographical Percussion of the Pulmonary Apices.—There are 
cases of incipient phthisis in which comparative percussion gives no 
conclusive information, and only topographical percussion—mapping 


ow 


{ 


bey 
ye 






rp 
< 


ie, 


wes) 
H} 


Pays 






Fic. 69.—Lung margins according to Goldscheider. 


out the limits of the apical resonance—may clear up the case. This 
can only be done intelligently when we have clear ideas as to the limits 
of these resonant areas in the healthy person. 

Kronig? showed that the resonant areas project as cones anteriorly 
and posteriorly, and that these two cones are united on the top of the 
shoulders by a narrow strip of resonance—the isthmus (Figs. 70 and 
71). With careful and very light percussion we can easily map out 
the mesial line which runs in front, beginning at the sternoclavicular 
articulation, upward and outward forming a concavity inward, while 


1 Berl. klin. Wehnschr., 1912, 49, 101. 
Deutsch. Klinik, 1907, 11, 581 and 634. 


326 PERCUSSION OF THE CHEST IN PHTHISIS 


posteriorly the line forms a convexity and ends at the level of the lower 
border of the second thoracic spinous process. The external line sepa- 
rating the resonant apex from the dull shoulder and neck runs from 
the middle of the anterior border of the trapezius, curving downward 
and reaching the clavicle at the junction of the middle and outer thirds 
and continuing obliquely downward toward the axilla; proceeding 
upward, it forms a convexity toward the neck, crossing the shoulders, 





Fie. 71 
TFias. 70 and 71.—Krénig’s apical resonant areas. 


on the top of which it is separated from the mesial line by a resonant 
space of about 2 or 3 cm. forming the isthmus, and proceeding down- 
ward with its concavity outward, terminating a couple of centimeters 
outside of the middle line of the scapula. Normally the height of the 
apex is anteriorly about 2 or 3 cm. above the clavicle, and posteriorly, 
on a level with the first thoracic spine, about 2 cm. outside of the 
middle line of the body. 


CHANGES IN APICAL RESONANCE IN PHTHISIS yA | 


It is important to remember that the pleximeter finger should be 
applied parallel with the line we expect to delineate; in this case at 
right angles with the clavicle. It is better to percuss from the lower 
parts of the chest upward, because in the former the normal note 
is usually found in early cases and it is always best to compare normal 
resonance with defective by striking the former first, as was already 
indicated. 

Changes in Apical Resonance in Phthisis.—When the resonant 
areas are marked out on the chest of a healthy person, their height 
and width are practically the same on both sides. But in phthisis one 
side will be found contracted. Recalling that a tuberculous lesion in 





Fig. 72.—Contraction of the resonant area of the left apex. 


the apex involves shrinkage of the pulmonary parenchyma, we have 
an explanation for this phenomenon. The extent of the shrinkage 
depends on many factors, mainly the degree of pulmonary retraction 
and the location of the lesion. When the lesion is centrally located, 
shrinkage of the apex is greater than when it is located at the periphery 
or under the pleura, as has been shown by Oestreich, obviously because 
in the former case traction is exerted on all sides. Autopsy findings 
show conclusively that this shrinkage occurs quite early, much earlier 
than is generally appreciated, and for this reason we may get a clear 
view as to the condition of the lung in that region, by percussing the 
apices and mapping out Kronig’s resonant areas. 


328 PERCUSSION OF THE CHEST IN PHTHISIS 


Shrinkage manifests itself in two ways: 

1. By a narrowing of the field of resonance on the affected side. 
This can be established by actual measurement. The isthmus in 
healthy persons is about 2 or 3 em. in width, and when we find it less 
than 1.5 cm. in width, it requires investigation. The width of the 
base of the resonant cone may be measured simply in finger-breadths, 
as has been recommended by R. N. Philip.!. Both sides are to be of 
the same width. 

2. By a blurring of the line separating the resonant from the dull 
parts (Figs. 73 and 74). While in health we can easily percuss out a 





Fie. 73.—Kronig’s resonant areas, showing a band of doubtful or relative resonance 
at the mesial border of the left apex; also retraction of the lower margin of the left 
lung. 


clear line of demarcation, in tuberculous apices there is often an 
interval in which the resonance is doubtful. This is mostly found at 
the inner outlines, but may be found at both sides. Kronig attributed 
it to changes in the tension of apical parenchyma at the margin of the 
affected parts. These points are better illustrated than described 
(Fig. 73), and in practice after the outlines of the apices have been 
marked out with a skin pencil, any existing differences in the outlines 
of the apices when one side is compared with the other are noted at 
a glance and need no measuring. 


1 Edinburgh Med. Jour., 1907, 22, 473. 


SOURCES OF ERROR 329 


Sources of Error.—rénig’s method is of excellent service in most 
cases of incipient phthisis. But we often meet with cases in which 
after careful and time-consuming work, the results attained are unsatis- 
factory. I have seen cases of phthisis in which no dislocation of any 
of the outlines of the apical resonance could be made out. Then 
there are numerous cases in which contraction of the apex is made 
out very nicely, but there is no active phthisis. This is especially 
true of “collapse induration,” which will be discussed later on. Healed 
tuberculous lesions also leave contracted apices and what we seek 
to determine is the presence of active phthisis. Walter C. Klotz found 
differences in the two sides very frequent in non-tuberculous indi- 





Fig. 74.—Bands of doubtful resonance on both sides of the right apex anteriorly. 


viduals; the right side is often narrower, regardless of the site of the 
most extensive lesion. His conclusion, which is in agreement with our 
experience, is to the effect that unless the disparity of the apical per- 
cussion field, expressed in terms of Krénig’s isthmus, is very marked, 
it does not necessarily point toward tuberculosis of the corresponding 
side. Such a disparity is also of less significance on the right side 
than on the left. 

Krénig stated that in phthisis the motion of the base is invariably 
affected at an early stage, while in non-tuberculous apical lesions 
the expansion of the lower margins of the lung remains normal. This 
does not hold in practice. There are many cases of phthisis in which 


330 PERCUSSION OF THE CHEST IN PHTHISIS 


the base retains its normal mobility during inspiration and expira- 
tion, and the reverse. The reason for the occasional failure of this 
method of percussion lies in the fact that the resonant area is not an 
outline of the true anatomical apex, but merely a projection of the 
same lung tissue in various directions (Figs. 77 and 78). The fact is 
that it is impossible to project the top of the lung on the surface of the 
body, considering its peculiar anatomical position and form. Krénig’s 
isthmus, for instance, does not exist at all, and we must remember 
that only the mesial border corresponds to the anatomical margin of 
the lung anteriorly and posteriorly. The lateral border cannot be 





Fia. 75.—Frequent findings with Krénig’s method of percussion in advanced cases. 
Retraction of the left lung. 


determined with exactness in most cases because the percussion wave 
strikes the spot tangentially. In patients with marked scoliosis, the 
method is of no value at all. 
Goldscheider’s Method of Apical Percussion.— Anatomical studies by 
Goldscheider,! as well as orthodiagraphic examination of the lungs 
in their relation to the bony thorax, show conclusively that there is 
no lung tissue in most of the resonant area percussed out by Kroénig’s 
method. Anteriorly, the apex lies beneath the two heads of the sterno- 
cleidomastoid, protruding above the inner third of the clavicle for 


1 Berl. klin. Wehnschr., 1907, 40, 1267 and 1309. 


GOLDSCHEIDER’S METHOD OF APICAL PERCUSSION 331 


about one inch in height. This is seen clinically when emaciated per- 
sons cough and the lung is blown up above the clavicle, or in wasted 
infants during crying spells. Posteriorly, the apex of the lung lies 
close to the spinal column, reaching as high as the spinous process 
of the first thoracic vertebra. But there it is impossible to obtain 
resonance from it because it is covered by a bony transverse process, 
rib and thick muscles. 

Goldscheider, for these anatomical reasons, devised another method 
of obtaining the resonance of the true anatomical apex, which we dis- 
cussed in detail elsewhere.2, From the complicated procedure of Gold- 
scheider all that is of utility in doubtful cases is the determination 


4 \7 ne, 


a re 
BS AN 4 
| 5) 
by MA 
7 \ 


/ I 


| 


Fia. 76.—Same patient as in Fig. 75; findings posteriorly, 


of the height of the apex between the heads of the sternocleidomas- 
toid, which can easily be done by percussing from below upward with 
the hooked finger as a pleximeter and comparing the two sides. Pos- 
teriorly, the lung resonance should reach the tip of the spinous process 
of the first thoracic vertebra on both sides. The height of the apices 
on both sides normally should be the same, and if it is found shorter 
on one side, it demands investigation as to the cause. In connection 
with other symptoms, it is strongly in favor of tuberculosis. But here 


1 Ztschr. f. klin. Med., 1910, 69, 205. 
2 New York Med. Jour., 1913, 97, 799. 


332 PERCUSSION OF THE CHEST IN PHTHISIS 


again, it may be an old, healed lesion. The distinction between active 
and healed lesions is made by means other than percussion. 

Tidal Percussion.— After ascertaining the limits of the apices, the 
base is to be delineated with a view of determining the vertical move- 
ments of the lung in the pleural sinus during both phases of respira- 
tion. This gives us information as to the presence or absence of 
emphysema, especially in fibroid phthisis, pleural adhesions, which 
are of such immense interest when contemplating the application of 
a therapeutic pneumothorax, etc. 





Fia. 77.—Showing that Krénig’s resonant areas are not outlines of the apical margins 
but are merely projections of the same lung tissue in various directions. (After Gold- 
scheider.) 


The lower margins of the lung resonance are first ascertained by 
percussion while the patient breathes normally and quietly, and marked 
with a dermographic pencil. Then the patient is directed to take a 
deep breath, and hold it as long as possible, while we again percuss 
and ascertain the lower limits of the lung, and again mark them with 
the pencil. In healthy persons the difference in these two lines is 
between one and two and a half inches. It is to be borne in mind that 
on the left side the lung margin is naturally about an inch lower 


PERCUSSION IN ADVANCED PHTHISIS 300 


than on the right; also that the expansion is greater in the axillary 
line anteriorly than posteriorly. In emphysematous subjects, also in 
the senile, and in those with deformed chests, expansion may be very 
little or nil. Pain while breathing may have the same effect. On 
the left side, when there is no expansion anteriorly at Traube’s semi- 
lunar space, it is an indication of pleural adhesions, or effusion; an 
increase in the tympany at that space indicates retraction of the left 
lung, not infrequent in phthisis. 





Fic. 78.—Showing that Kroénig’s resonant areas are not outlines of the apical margins, 
but are merely projections of the same lung tissue in various directions. In the supra- 
spinous fosse there is no lung tissue at all. (After Goldscheider.) 


In most cases of incipient phthisis the respiratory excursion of the 
affected lung is more or less restricted, and when there are adhesions, 
there is unilateral absence of respiratory excursions. But since we 
have been interested in pleural adhesions while making artificial 
pneumothorax, we find that these signs are not absolutely reliable. 

Percussion in Advanced Phthisis.— With the advance of the disease 
the percussion findings become more and more varied and scattered 
all over the chest, and the difficulties of determining the exact condi- 
tion of the lungs from percussion findings alone, more and more unsur- 


04 PERCUSSION OF THE CHEST IN PHTHISIS 


-~mountable. The dulness elicited is usually due not only to the active 
lesions, but also to such as have healed or are quiescent; to thickened 
pleura, which is usually a conservative process; to pleural effusions, 
displacements of the heart, diaphragm, liver, stomach, etc. Some 
of these processes are permanent, others appear for a short time and 
disappear. Localized emphysema, transient or permanent, due to 
vicarious function, often obscures deeply lying airless tissue. 

In most cases, however, we find that one lung shows dense dulness 
in its upper part, usually as far as the third or fourth rib, as well as 
retraction of one or, more rarely, both bases. Put even this may be 





Y 


Fic. 79.—Topography of the apex according to Goldscheider: upper and mesial 
borders of the lung; - -- - - borders of the first rib and clavicle. On the left side the 
clavicular head of the sternocleidomastoid has been removed so that the sealenus anticus 
is visible. The upper border of the lung is somewhat higher than the first rib. 





due to healed or quiescent old lesions. We also find a frequent area 
of dulness in one and, at times, in both interscapular spaces due to 
lesions of the apices of the lower lobes, or enlarged glands. At times 
the dulness runs along the lines of the interlobar fissures anteriorly and 
posteriorly. To map out such areas of dulness may be of scientific 
interest, but the diagnosis of these cases rests on other methods of 
exploration, especially the subjective symptoms. Signs of excavation 
are discussed elsewhere. (See Chapter XX.) 

Sources of Error in Signs Elicited by Percussion.— When finding 
defective resonance over one apex, contraction of Kr6énig’s resonant 
area on one side, or one apex shorter than the other, thus indicating 


DIAGNOSTIC VALUE OF PERCUSSION 330 


pulmonary retraction, are we justified in considering the patient sick 
with active phthisis? Are differences in resonance elicited when the 
two sides of the chest are symmetrically and comparatively percussed, 
especially in its upper third, sure indications of active phthisis? 

These problems confront the clinician quite often, and they can 
only be answered by an intelligent consideration of the causes of 
defective resonance and dulness, which are mainly airless lung tissue, 
and which may be due to many causes in addition to tuberculosis. 
Besides, we may have differences in the resonance due to faulty technic 
in percussion, also because of asymmetry of the chest in cases of 
kyphosis or scoliosis, or unilateral hypertrophy of the muscles due to 
occupational effects. These facts are to be borne in mind while we 
attempt to interpret percussion findings in early phthisis. 

There are other sources of error. Chronic pneumonic processes, 
healed apical lesions and pleurisy are very common, as we have 
already shown, and many leave some airless tissue which is detected 
by careful percussion. So that even if due to tuberculosis, apical 
dulness or retraction does not always mean active phthisis requiring 
therapeutic intervention. Collapse induration, due to inhalation of 
dust in mouth-breathers, may show percussion signs which are undis- 
tinguishable from phthisis, if we should rely on percussion alone. 
We also occasionally find dulness in the apices in persons leading 
a sedentary life, and who do not breathe deeply, especially chlorotic 
girls. Some of these cases are cleared up by directing the patient to 
breathe deeply for some minutes, or practising Da Costa’s respiratory 
percussion. 

We also meet now and then with persons in whom the resonance 
on one or both sides of the chest is defective without any excessive 
adiposity or strongly developed muscles to account for it. The air 
content of the lungs is less in childhood than in later life, and it decreases 
with old age, often without showing any anatomical changes in the 
lungs at the autopsy. 

In many cases a study of the overlying muscles as to rigidity and 
atrophy has helped me immensely, while in others it was of no avail. 

Diagnostic Value of Percussion.—In cases presenting symptoms of 
phthisis such as fever, cough, nightsweats, etc., percussion findings 
alone are often sufficient to localize the lesion, and in many cases it 
will be found by prolonged observation that a lesion develops in the 
apex where we originally found only defective resonance or contrac- 
tion of the field of resonance, though auscultatory signs were wanting. 

Percussion findings alone, without any general symptoms of phthisis, 
are not conclusive, just as in roentgenography a shadow over an apex 
does not prove an active tuberculous lesion. It is only in connection 
with constitutional symptoms that percussion, like any other single 
sign, can be utilized for diagnosis. 

However, whenever found, defective resonance in an apex demands 
careful investigation and watching of the case until a reason is found 
for its existence, 


CHA PTE RX VL 
AUSCULTATION OF THE CHEST IN PHTHISIS. 


WE have shown that percussion is a most valuable diagnostic method 
in early phthisis, even more valuable than in the later stages, and will 
often give definite information as to the air content of the lungs much 
earlier than other methods. Auscultation is just as valuable for 
other reasons. At times it affords information in cases in which the 
lesion is centrally located, and in tuberculosis grafted on an emphy- 
sematous lung, when percussion and even roentgenography may 
fail. Similarly, in advanced cases where the lesion is extending, altered 
breath sounds and rales may often be found in advance of dulness. 
On the other hand, acute cases, especially miliary tuberculosis, may 
show normal breath sounds and no rales, and in chronic cases with 
deeply lying cavities the normal lung tissue conceals the signs of 
excavation. In the former diffuse tympany, while in the latter per- 
cussion or roentgenography, may disclose the exact state of affairs. 

Believing that the technic of auscultation is much easier to master 
than that of percussion, many have discarded the latter and rely 
solely on the former, which is a grave error. The fact is that dt is just 
as difficult to acquire skill in proper auscultation of the chest, and in 
interpreting the findings correctly, as to percuss properly. Some, like 
Goldscheider! and Clive Riviere,” believe that auscultation is even more 
difficult to master. It is because of faulty technic that auscultation 
does not yield all the information that can be obtained by this method. 

Technic of Auscultation.—The patient should be stripped to the 
waist, just as for percussion, and seated on a high revolving stool, 
so as to be accessible from all sides. Before beginning auscultation 
the physician must assure himself that the patient knows how to 
breathe properly and if not, which is very often the case, proper 
instruction is to be given objectively. One important drawback to 
auscultation is that many patients do not know how to exhale—they 
just inspire jerkily, and stop with inflated chests. Others, usually 
such as have led a sedentary life and never expanded their chests 
properly; inhale and exhale quickly in rapid succession so that it is 
difficult to follow each phase of respiration. While in the vast majority 
a little instruction suffices, at times we meet with some, and not 
exclusively among those reputed to be ignorant, who will not breathe 
properly for our purposes, especially nervous individuals, and the 


1 Ztschr. f. klin. Medizin., 1910, 69, 205. 


» Early Diagnosis of Tubercle, London, 1914, p. 22. 


SINGLE PHASE AUSCULTATION Boal 


examination must be postponed till they become accustomed to the 
physician. 

The breathing must be regular, rhythmic, somewhat deeper than 
usual, and preferably through the nose, because when the air enters 
this way the lungs expand much better and more uniformly. Mouth- 
breathing occasionally induces cough. In cases of nasal obstruction 
the patient breathes through his mouth, but we must guard against 
noises arising in the pharynx, especially those created by the soft palate, 
which impart a bronchial or blowing character to the breath sounds and, 
at times, give an impression of prolonged expiratory murmur, when 
in fact there is nothing of the kind. 

Special attention should be paid to expiration, during which the 
patient should empty his chest as much as possible, without any 
undue exertion, and that each expiration should promptly be followed 
by a deep inspiration. 

Any stethoscope to which the physician is accustomed may be 
used. The writer prefers the Bowles model, and the one devised by 
J. J. Singer, of St. Louis, has given satisfaction. The bell should be 
applied carefully in the intercostal spaces, especially in emaciated 
persons, so that it makes an air-tight connection with the skin. It 
should be held firmly but without any undue pressure, thus excluding 
all extraneous noises. Movement of the bell of the stethoscope upon 
the surface of the body interferes greatly with proper auscultation 
and should be avoided. 

Single Phase Auscultation.—'l’o appreciate slight changes in the 
duration and quality of the respiratory murmur it is important to 
listen to each phase of the respiratory act separately. Grancher’s! 
method has served me best. It consists in first listening to the inspira- 
tory murmur and to neglect at the time the expiratory murmur; and 
when listening to the latter the former is to be neglected. Rales are 
always looked for separately, after we have a clear idea as to the 
character of the breath sounds. 

Beginning, for instance, with auscultation of the left apex, we 
listen attentively to the inspiratory murmur, and while the patient 
exhales, the bell of the stethoscope is quickly carried over to a cor- 
responding point on the right side of the chest, and we listen to an 
inspiration. The inspiratory murmur is thus compared right and 
left, and any differences that may be found are carefully noted. In 
this manner the slightest change in the murmur on one side can be 
best appreciated, because we have a-standard in the unaffected side. 
Only when both sides of the chest are affected is this method unin- 
structive, because we do not have an immediate impression of a normal 
inspiratory murmur. The expiratory murmur is to be studied in the 
same manner, carrying over the bell of the stethoscope while the 
patient inspires, and noting the difference. While listening to these 


1 Maladies de l'appareil respiratoire, Paris, 1890. 
22 


338 AUSCULTATION OF THE CHEST IN PHTHISIS 


murmurs, no attention at all is paid to any adventitious sounds which 
may be present. ‘These are left for separate study. 

This method of auscultation, devised by Grancher, and hardly ever 
mentioned in our text-books, is the only one that can bring out all the 
changes in the respiratory murmur heard in really incipient pulmonary 
lesions, and should be used exclusively. 

The Normal Respiratory Murmurs.—The most important prerequi- 
site of proper interpretation of auscultatory findings in pathological 
conditions of the lungs is a knowledge of, and experience with, the 
respiratory murmur audible in normal chests. Without this knowl- 
edge we cannot expect to appreciate slight changes audible during 
either phase of the respiratory act in early phthisis. It is because of 
the disregard of the qualities of the physiological breath sounds that 
slight changes are overlooked, and many state that only with the 
appearance of adventitious sounds can a positive diagnosis be made, 
which is decidedly wrong, just as is waiting for tubercle bacilli to make 
their appearance in the sputum. One who wants to appreciate the 
early changes of phthisis cannot auscultate normal chests too often. 

The physiological, or vesicular, respiratory murmur shows that the 
pulmonary parenchyma at the auscultated area contains air which 
enters with each act of inspiration and leaves with each act of expira- 
tion without meeting any obstruction in its course. During inspira- 
tion it is audible with different degrees of intensity all over the chest 
as a sighing, whispering rustle; during expiration there is either no 
murmur at all, or, more commonly, a very faint noise is heard which 
is somewhat lower pitched than, and it lasts but one-fifth the time 
of, the inspiratory murmur, notwithstanding that expiration actually 
lasts longer than inspiration. 

Without entering into the problem of the origin of these murmurs, 
whether they are produced in the glottis or in the air cells in the 
areas under examination, we want to emphasize that it is important 
to bear in mind while auscultating that any changes in pitch, quality 
and rhythm noted during either phase of respiration are to be given 
careful attention in cases in which early phthisis is suspected. 

Feeble Breathing.— When meeting a patient with a really incipient 
lesion, which is not often our privilege because when they present 
themselves the lesion is usually more advanced than is generally appre- 
ciated, we find no adventitious sounds, no changes in the type of 
breathing, no bronchovesicular or bronchial breathing, etc. The 
most common change in the breath sounds at this stage is feeble 
breathing, or, more rarely, complete absence of the respiratory mur- 
mur over a circumscribed area in one of the apices, mostly found 
posteriorly near or above the spine of the scapula, the zone d’alarme 
of some French authors,! and anteriorly beneath the inner third of the 
clavicle. At times this feeble murmur is blowing or even bronchial in 


* Sergent, Le Monde Médical, 1912, 22, 1121; La Clinique, 1913, 8, 437. 


FEEBLE BREATHING | 339 


character and at the end of inspiration some dry crackling may be 
heard. 

It is noteworthy that while very few modern authors mention feeble 
breath sounds in incipient tuberculosis, the great French clinician of the 
first half of the nineteenth century, Andral, already considered it a good 
and reliable sign. He says: ‘We have ascertained weakness of the 
respiratory murmur, or even its total absence, in points where, after 
death, we found tubercles scattered in greater or less number in the 
midst of the pulmonary parenchyma very much indurated, and became 
entirely impermeable to the air.”’ 

To be of diagnostic significance this feeble breathing must be localized 
over one apex, circumscribed, fixed and persistent for some time, and 
uninfluenced by respiratory efforts and cough. It is an indication of 
peribronchial tuberculous infiltration compressing some bronchioles, 
thus creating atelectasis of the alveoli they supply; or of localized 
pleurisy interfering with the respiratory activity of the alveoli in the 
affected area. 

“In massive caseation,” says Colonel Bushnell, “the tissues have 
lost their elasticity and, in so far as they are caseated, do not expand at 
all in inspiration. Ordinary breath sounds are absent in such cases, or 
are present enfeebled in less complete caseations. Ordinarily what is 
heard is a weak and distant bronchial breathing, conducted from the 
deep bronchi and mingled with the coarse rales characteristic of these 
tubes.” 

Localized feeble breath sounds are also found over healed tuber- 
culous lesions, or adhesions of the apical pleura following abortive 
tuberculosis. But during the early stage of active phthisis feeble 
breathing is accompanied by constitutional symptoms, such as cough, 
fever, tachycardia, etc., and usually some signs are elicited by percus- 
sion of the same area. As Bezancon! has pointed out, an the absence 
of constitutional symptoms, feeble breathing at one apex is a sign of a 
healed tuberculous lesion. 

In advanced phthisis, we very often meet with limited areas of 
feeble or absent breathing, but vigorous cough removes the plug which 
obstructs the entry of air into a bronchus and breath sounds are again 
audible. It is noteworthy and of diagnostic importance that atelec- 
tasis is frequently produced by plugging of a bronchus and the result- 
ing resorption of the air from the alveoli may produce dulness over 
the area supplied by that bronchus, but no breath sounds, no adven- 
titious sounds are heard. Occurring at the base, it is often difficult 
to distinguish it from thickened or adherent pleura, which is also 
characterized by feeble or absent breathing, as is pleural exudate. 
Likewise, over old bronchiectatic cavities, the breath sounds are often 
lacking or are feeble, though the rales are quite pronounced, consonating. 

In acute pneumonic phthisis I have repeatedly met feeble breath 


1 Rev. de la tuberculose, 1913, 10, 1. 


340 AUSCULTATION OF THE CHEST IN PHTHISIS 


sounds in addition to dulness elicited over the affected lobe of the 
lung; at times there was even absence of all breath murmurs, but 
some moist suberepitant rales were audible over the same region. 
Similarly, we may meet, during febrile exacerbations in advanced 
cases, feeble breathing over newly affected areas, which later changes 
into bronchial breathing, ete. 

Rough or Granular Breathing.—This is often found in incipient 
cases. Here again it is the inspiratory murmur that is especially 
affected. It is dry, rough and low-pitched. It should not be con- 
founded with puerile or harsh breathing: Granular breathing may be 
altogether diminished in intensity, or even very faint, while puerile 
breathing is always intense and emphatically pure. On the other hand, 
in granular breathing there is always a suspicion that adventitious 
sounds or noises are superadding the inspiratory murmur. According 
to Sahli, it is a sign of bronchial catarrh; there is either partial imper- 
meability of the bronchi producing unequal respiratory excursions of 
the affected lung area, or else the accompanying noises are derived from 
the secretions causing partial stenosis or irregularity in the lumen. 
When these accompanying noises can be plainly isolated we call them 
rales, but as they remain indistinct and blended, the vesicular breath- 
ing becomes impure, granular or rough. It is generally heard over the 
supraspinous fosse, or above and beneath the clavicle. 

As has been pointed out by Bray,! for a satisfactory demonstration 
of granular breathing at the apex, the muscles of this region must be 
in a state of relaxaction, because their active contraction may at times 
produce sounds indistinguishable from granular breathing, and thus 
lead to confusion in diagnosis. | He suggests to listen while the patient 
breathes abdominally. In this type of breathing, respiration is con- 
ducted solely by the piston-like excursions of the diaphragm, the thorax 
is fixed, and the muscles in the region of the apex relaxed. Only when 
granular breathing is heard while the patient breathes abdominally, 
thus eliminating extrapulmonary sounds, is one justified in concluding 
that the vesicular murmur has undergone a definite pathological 
alteration. 

Grancher insists that granular breathing is a sure sign of incipient 
phthisis, and Clive Riviere speaks of it as the earliest auscultatory 
sign, while Piéry? says that it is nothing of the k'nd, but that it is a 
good sign of a cured lesion and due to cicatrization of a limited area of 
lung tissue, which is undoubtedly a fact. I have seen many patients 
who presented granular breathing at an apex for years without showing 
any of the constitutional symptoms of phthisis. On the other hand, I 
have full confidence in this sign when there are the usual general symp- 
toms of phthisis, because I have repeatedly observed that in the very 
area first presenting feeble or granular breathing there subsequently 
developed typical lesions of phthisis. Of course, one must always bear 


1 Jour. Am. Med. Assn., 1917, 69, 1762. 
2 La tuberculose pulmonaire, Paris, 1910, p. 311. 


PROLONGED EXPIRATION 341 


in mind that the absence of constitutional symptoms is an indication 
that the granular breathing is probably due to a cicatrix remaining after 
a tuberculous lesion has healed. 

Interrupted or Cog-wheel Breathing.—The respiration saccadée of 
the French is another anomalous type of breath sounds which has 
for a long time been considered characteristic of early phthisis. The 
inspiratory murmur is not smooth and continuous, as in normal respira- 
tion, but is broken, so that it appears jerky, divided into several more 
or less distinct parts. It differs from rough breathing by the fact that 
each portion of the sound retains its smooth, rustling character. It 
is apparently caused by the obstacles met by the air current while 
entering the alveoli. The breath sounds may be increased or, more 
commonly, decreased in intensity. 

I find cog-wheel respiration only rarely a sign of incipient phthisis 
and am inclined to agree with Piéry, who says that in the region of 
the apex it is always an indication of pleural adhesions which are 
often the remains of a healed tuberculous lesion. In some cases, 
however, it is met with in the beginning of active phthisis and the 
fact that in the later stages of the disease it can very often be heard 
along the borders of advancing lesions shows that the factors pro- 
ducing it may be of the first disturbances of the respiratory murmur 
in the areas of impaired breathing capacity around infiltrated portions 
of the lung. 

Cog-wheel breathing is occasionally heard over chests in nervous 
patients, or such as have pains due to acute pleurisy, or who shiver 
during the examination. But then it is heard all over the chest, while 
in phthisis it is localized over a limited area. 

Prolonged Expiration.—From what has been stated it is evident 
that in the very early stages of phthisis, auscultation reveals only changes 
in the inspiratory murmur, a point which cannot be too strongly empha- 
sized. In older books on the subject we almost always read that 
changes in the expiratory murmur are pathognomonic of early phthisis, 
obviously because in former days incipient phthisis, as we know it 
today, was not recognized. In fact, because even today patients only 
rarely present themselves for examination at the very incipiency of the 
disease, we usually find a prolonged expiratory murmur at the first 
examination. But speakingas one who has had opportunities for exami- 
nation of large numbers of persons who do not even suspect that they 
have any pulmonary trouble, and examining the lungs of everyone 
who comes under my care, I find that changes in the inspiratory mur- 
mur, such as feeble breath sounds, rough or cog-wheel breathing, are 
usually found earlier than changes in the expiratory murmur. 

In normal vesicular breathing the expiratory murmur is either 
inaudible or, more commonly, it lasts only one-fifth to one-fourth the 
time of the inspiratory murmur. When it lasts as long as, or longer 
than, the inspiratory murmur it is undoubtedly pathological, though 
not necessarily of tuberculous origin. When audible all over the chest 


342 AUSCULTATION OF THE CHEST IN PHTHISIS 


it is an indication of bronchitis or pulmonary emphysema, but when 
we find it localized at one apex, its significance as a sign of phthisis 
is to be appreciated. It may be due to sclerosis of a limited portion 
of lung tissue, as is the case in healed tuberculous lesions. Indeed, 
when it also has a bronchial timber it is pathognomonic of this con- 
dition, and Turban speaks of it as “cicatricial respiration.” 

In active early lesions, a prolonged expiratory murmur, localized at 
an apex, is an indication of either catarrh of the smaller bronchioles, 
or pressure on these tubes, in cases in which infiltrations produce 
stenosis. It is therefore usually met with later than the changes in 
the inspiratory murmur, of which we spoke above. The prolonged 
expiratory murmur is often harsh and rough, and with the advance of 
the disease, it gradually acquires a bronchial character, finally becom- 
ing pure bronchial or tubular breathing. While we may meet it with- 
out any adventitious’ sounds, this is exceptional in my experience. 
On the other hand, it may be feeble and hardly audible and, at times, 
we hear the rales very clearly while the prolonged expiration is so feeble 
that it is only detected after careful listening. 

There is another fact to be borne in mind while evaluating prolonged 
expiration as a sign of early phthisis. Not only may it be the sole 
indication of a healed lesion, as has already been stated, but in the 
right apex it may not be due to tuberculosis at all, especially in young 
adults with thin thoracic walls. In collapse induration it is not uncom- 
mon, while in persons working at dusty trades, such as stone-cutters, 
carpenters, miners, garment-workers, etc., the expiratory murmur at 
the right apex is very often harsh, rough and prolonged. Under the 
circumstances it is of more significance when found in the left apex, 
and in the right side a careful study of the constitutional symptoms 
must be made before attaching any diagnostic value to it. 

Bronchial Breathing.—With the advance of the disease the dis- 
seminated tubercles in the lung conglomerate by growth and form a 
solid circumscribed mass, over which the breath sounds elicited on 
auscultation are more or less characteristic. The vesicular quality 
of the murmur changes by degrees, till it finally becomes high-pitched, 
clear and blowing during both inspiration and expiration, which is 
very prolonged. 

Bronchial breathing is a sign of consolidation of lung tissue: The 
laryngotracheal murmur is transmitted and, according to Sahli, even 
magnified, while passing from the bronchi through consolidated lung 
tissue to the surface. It is thus heard over areas which are dull on 
percussion, particularly over the upper third of the chest anteriorly 
and posteriorly. During the course of chronic phthisis bronchial 
breathing is also caused by many complications which produce com- 
pression of the alveoli with resulting pulmonary atelectasis, as is the 
case in pleural effusions, pneumothorax, hydrothorax, etc. In these 
cases the bronchial breathing is engendered only when the alveoli and, 
at most, the bronchioles are compressed; when the large tubes are also 
obliterated by compression, no breath sounds at all are audible. 


BRONCHOVESICULAR BREATHING 343 


In acute phthisis, bronchial breathing is mainly caused by caseous 
infiltration of the affected areas, and it is harsher, louder and more 
high-pitched, the more compact and extensive the consolidation of 
lung tissue. Bronchial breathing in phthisis is not so loud and high- 
pitched as in pneumonia, and when it is encountered, it is an indication 
of an acute process which is probably progressive and of serious 
prognostic significance. It is therefore found early in the disease in 
acute pneumonic phthisis and during chronic phthisis over the seat of 
new extensions of the process, involving the larger part of a lobe, and 
in the terminal stages, when tuberculous bronchopneumonia compli- 
cates an old lesion and carries off the patient. In chronic phthisis, 
the higher the pitch of bronchial breathing, the greater the consoli- 
dation of lung tissue may be assumed. 

It is a fact to be remembered that in the average case of chronic 
phthisis bronchial breathing does not appear suddenly but by slow 
degrees. The vesicular murmur is gradually transformed into broncho- 
vesicular, which, with the subsequent consolidation of the process, 
finally becomes purely bronchial. 

Bronchovesicular Breathing.—On rare occasions, we may find 
bronchial breathing with normal resonance over the same area; in fact, 
I have at times met it over areas emitting a tympanitic note on per- 
cussion, which is an indication that even small disseminated tubercles, 
which are incapable of producing dulness, but relax the lung tissue 
and cause tympany, may cause bronchial breathing. 

But usually disseminated tubercles produce bronchovesicular breath- 
ing. We hear a mixture of both vesicular and bronchial sounds over 
the same area, the former originating in the small consolidated areas 
which transmit the laryngotracheal sounds, while the latter come from 
the alveoli of the unaffected lung tissue that surrounds the tubercles. 
It is thus clear that the presence of bronchovesicular breathing is an 
indication of small tubercles scattered within normal lung tissue. 
This is usually preceded by prolonged expiration, which changes by 
degrees into bronchovesicular breathing, and finally into bronchial, 
as has already been shown 

Bray, however, offers another ingenious explanation of the origin 
of bronchovesicular breathing. He points out that the lung glides 
beneath the ribs during respiration, and as a result the lung surface 
auscultated over any given area is considerably greater than that repre- 
sented by the bell of the stethoscope. The area of lung ausculta- 
ted will thus vary with the motion of the lung. Bronchovesicular breath 
sounds are heard when there are contiguous areas of consolidated and 
air containing lung tissue, which alternately pass across the auscultated 
field during respiration. 

Sources of Error.— Bronchial and bronchovesicular breathing per se 
are no indications of phthisis. In addition to the many pathological 
conditions which may cause this type of breath sounds, we quite 
often hear it over healthy chests. There are many individuals in 


344 AUSCULTATION OF THE CHEST IN PHTHISIS 


whom bronchial breathing is heard all over the upper parts of the 
thorax. In the interscapular, right supraspinous and supraclavicular 
spaces it is very common in apparently healthy persons, especially 
during vigorous breathing. This is said by Bandelier and Répke to 
be found in about one-third of healthy people; it is due to differences 
in the anatomical structure of the two apices. The right lung has 
three main bronchi, which favor the transmission of bronchial breathing 
more than the left, which has only two. It will be noted (Fig. 80) 
that,the branches of the bronchus supplying the right apex are wider 
and go deeper into the parenchyma, thus affording better opportunities 
for transmission of sound to the surface, than in the left apex. 





Frg. 80.—Topographical relations of the large bronchi and pulmonary bloodvessels 
after removal of the posterior wall of the thorax, the esophagus and descending aorta. 
Pulmonary artery dark; pulmonary vein light. (Stoerck.) 


Bronchial breathing is very common in these locations and is not 
to be given undue diagnostic significance unless there are other symp- 
toms and signs of phthisis. Individuals with thin thoracic walls are 
more apt to show this sort of breath sounds, while vigorous breathing 
and dyspnea may accentuate it. To be of diagnostic significance, 
bronchial breathing must be strictly localized over a limited area and 
accompanied by other physical signs, especially dulness at the same spot. 

Another source of error in auscultation is the frequent changes we 
meet'in the respiratory sounds in many patients. One day we meet 
at the affected area bronchial breathing, and the next day we are 
surprised by vesicular or feeble breathing, or complete absence of 


ADVENTITIOUS SOUNDS 345 


breath sounds over the very area where distinct pathological auscul- 
tatory phenomena were audible the day before. Vigorous cough, by 
removing the mucous plug in some tube, may reéstablish the original 
sounds. I have seen such changes occurring during an examination 
which lasted less than half an hour. We should therefore beware 
of pronouncing a patient free from changes in the breath sounds 
before making him cough, and reéxamining the chest on several different 
days. 

Cavernous and amphoric breathing are discussed later when speaking 
of pulmonary excavations and of pneumothorax. 

Adventitious Sounds.—<As was already stated while speaking of the 
technic of auscultation, adventitious sounds are to be looked for only 
after ascertaining the character of the breath sounds during each 
phase of the respiratory act. To pass judgment at the same time about 
both, breath sounds and rales is hazardous and we are liable to over- 
look many important points which are of diagnostic and prognostic 
significance. 

The adventitious sounds audible over phthisical chests in the various 
stages of the disease are manifold. It can be stated that all kinds of 
rales—sonorous, sibilant, crepitant, subcrepitant, gurgling, etc.—are 
met with during the course of the disease, and each variety has some 
significance, indicating various pathological conditions of the lung. 
Paradoxical though it may seem at first sight, yet it is a fact that there 
are no rales which are pathognomonic of phthisis, nor does their absence 
exclude the disease. Especially is this true of the very incipience of 
active phthisis which, as was already intimated, begins as an infil- 
tration and not as a catarrh of the bronchi. The neoplastic peri- 
bronchial formations may compress the alveoli; the proliferated 
interstitial tissues may contract and obliterate some air cells, etc., 
but such processes do not produce rales because at this stage the 
bronchi are not flooded with fluid or semifluid secretions which could 
interfere with the entry or exit of air through the bronchioles and air 
cells. Moreover, around an infiltrated area the lung usually acts 
vicariously, and thus veils any alteration in the breath sounds that may 
be created in the diseased focus, and the most we may expect is feeble, 
harsh, or cog-wheel breathing, but no rales. 

Rales are produced when the caseous material softens and breaks 
through the walls of a bronchus: The secretions may irritate the 
bronchial mucous membrane and produce a catarrh which, in its 
turn, produces more secretion which, when set in motion by the 
passing air stream, engenders rales. This is a fact that I have had 
many opportunities to observe in patients who, at first, showed only 
alterations in the breath sounds, especially weak vesicular murmur, 
or cog-wheel breathing, etc., but no rales, in spite of all constitutional 
symptoms of phthisis which went on its course, and only later adven- 
titious sounds made their appearance. In such cases a diagnosis of 
phthisis must be made without finding any rales. In fact, I have met 








346 AUSCULTATION OF THE CHEST IN PHTHISIS 


with acute cases in which a whole lobe was infiltrated in a compara- 
tively short time; percussion showed distinct dulness, auscultation 
disclosed prolonged expiration, even bronchial breathing, but no 
rales at all were audible. It will therefore bear repetition that wazting 
for rales, as some teat-books teach, may be worse than waiting for tubercle 
bacilli in the sputum before making a diagnosis. 

It is worthy of mention that while rales are an indication that the 
tuberculous process is beyond incipiency, they do not invariably 
point toward an unfavorable prognosis. ‘“‘ Rales constitute the auscul- 
tatory evidence of inflammatory reaction to the poisons of tubercle,”’ 
says Colonel Bushnell. “They are the best evidence that the lesion is 
resisting its foe. ales are absent in the obsolete or arrested lesion— 
the body does not need to fight. They are present in the stage of reac- 
tion—the body is fighting—whether successfully or not is to be deter- 
mined in part by the number and quality of the rales, in part by other 
considerations. ‘They may be absent again when the body can no 
longer fight—when the power to react has been lost. Nothing could 
be more erroneous than to draw favorable conclusions from the diminu- 
tion or the disappearance of rales in the very advanced case.”’ 

Crepitation.—With the onset of softening, the crepitant and, at 
times, the subcrepitant rale can be discovered at the affected area. 
The former is audible exclusively during inspiration, or only at its 
end, and has been compared to the sound produced by rolling one’s 
hair between the fingers near the ear. All agree that this rale is not 
caused by the motion of fluid secretions in the small bronchi and air 
cells; nor by the explosion of air bubbles in the bronchi, as was for- 
merly supposed. The consensus of opinion appears to be that it is 
caused by the inspiratory stream of air tearing apart sticky surfaces 
of the approximated alveolar walls, though many hold that the crepi- 
tant rale is altogether a friction sound produced by rubbing of the 
two pleural sheets covered with tubercles, as was first suggested by 
Leaming.! I am inclined to consider them purely atelectatic rales, 
analogous to those met with over the margins of healthy lungs in per- 
sons who breathe superficially, and which are often mistaken for 
crepitations. On the other hand, considering that apical tuberculous 
pleurisy is quite frequent (see page 486), these adventitious sounds 
are not infrequently due to frictions. The differentiation between 
pleural and parenchymatous lesions is discussed elsewhere. 

Crepitant rales are usually audible during quiet breathing, and 
provoked by vigorous coughing and breathing. Moreover, they often 
disappear after several strong efforts at deep breathing, which would 
not be the case if they were friction sounds. They may be found 
early in the morning, and missed throughout the day, and I have 
seen them appear and disappear within half an hour during an exami- 
nation. At times, they are heard at a very early stage of the disease 


1 Diseases of the Heart and Lungs, New York, 1884. 


MOIST RALES 347 


as quite numerous cracklings over the affected area, while in other 
cases but few are audible, and they are spoken of as “dry crackles,” 
the craquements secs of French authors. 

Crepitant rales are not by any means pathognomonic of phthisis, for 
reasons already stated, but when audible over an apex showing contrac- 
tion of Krénig’s resonant areas, or impaired resonance in a person show- 
ing some of the important constitutional symptoms of phthisis, they are 
to be taken seriously. However, in order to evaluate them properly, 
we must carefully study them with particular reference as to per- 
manence during several examinations on different days and that cough 
does not entirely remove them. I attach greater significance to crepi- 
tant rales when heard over the supraspinous fossa, the alarm zone (see 
p. 379), than when heard anteriorly, above, or immediately below the 
clavicle, because in the latter location they are as often spurious as 
real. We are often able to follow them up to the stage when they 
become moist—subcrepitant—and finally we find that signs of exca- 
vation appear at the same spot. 

During the course of phthisis, the crepitant rale is heard quite 
often around the seat of the main lesion, indicating that the process 
is extending, and over pneumonic areas so often caused by acute 
exacerbations. In unilateral cases, in which the other side is second- 
arily implicated, we may find that in the latter the first audible adven- 
titious sounds are crepitations, and these secondary lesions are worthy 
of study by those who want to be able to recognize and evaluate these 
adventitious sounds. In fact, while teaching tuberculosis to students, 
advanced cases are better for this reason than early cases in which the 
diagnosis is often doubtful. 

Moist Rales.— With the advance of the process, softening sets in 
and the disintegrated tubercles are eliminated from the focus through 
the bronchi, to be finally expectorated. These fluid and semifluid 
secretions, while remaining at the site of the lesion and in the bronchi, 
are often obstacles to the entry and exit of the air current and thus 
produce rales. In mild cases with but little secretion, we meet with 
the high-pitched subcrepitant rales produced in the small bronchi. 
When softening and liquefaction proceed and the secretions become 
more and more copious, the size of the rales increases and we hear 
medium, large and coarse bubbling rales and gurgles. 

The difference in the size of the rales apparently depends on the 
difference in the size of the bronchi in which they originate—large 
bronchi can hold larger masses of fluid and mucous secretion, and in 
smaller tubes less secretions are moved, while in excavations the 
mass of secretion may be very large and, as a result, we get gurgles. 
One way to differentiate between coarse and small rales is to note their 
number—we commonly hear but few isolated coarse rales, while small 
ones are almost always in large numbers, heaps. ‘The larger rales are 
more intense and louder, though of a lower pitch than the smaller, but 
the latter are usually more numerous, evidently because there are more 


348 AUSCULTATION OF THE CHEST IN PHTHISIS 


small bronchi than large ones. Rales are greater in number, and more 
consonating, when originating superficially, while those engendered 
deeply in the lung may not be heard at all. At times, we can hear 
rales in central lesions by placing the bell of the stethoscope in front of 
the patient’s mouth, while all over the chest nothing is audible. 

Consonating Rales.—As a rule, rales which originate in air-contain- 
ing lung tissue are only faintly audible, appear distant from the ear or 
stethoscope, and are therefore called non-consonating. When adventi- 
tious sounds are heard very near the surface of the chest, have a more 
or less ringing quality, which is lacking in the non-consonating variety, 
they are called consonating rales; at times they possess a metallic 
quality, and they are designated as gurgles, or bubbling rales. 

Consonating rales indicate consolidated lung tissue, a cavity or a 
dilated bronchus surrounded by airless tissue which either intensifies 
or modifies the timber of the sounds. For this reason they are at 
times ringing in character. On the whole it is difficult to describe them, 
but once heard they should not be missed in other cases. As has been 
shown by Sahli, better conduction through consolidated tissue is not 
alone sufficient to make the rale consonant; nor is loudness thus effec- 
tive. Tracheal rales may be loud enough to be heard at a distance, 
yet they are not consonant. The consonating character apparently 
depends on an admixture of the higher overtones. 

It may be stated that consonating ralés are engendered under the 
same circumstances as vs bronchial breathing. They are therefore indicat- 
ing that the area over which they are heard is either consolidated or exca- 
vated. When a cavity is surrounded by consolidated lung tissue, the 
rales are consonating; when it is deeply seated in air-containing lung, 
the rales are non-consonating in character. When the cavity is large, 
and the secretion within them is plentiful and mobile during respiration, 
consolidated lung tissue around it will so intensify the sounds as to 
produce bubbling or gurgling rales. 

Localization of Moist Rales.—It must be emphasized that no rales 
per se are pathognomonic of phthisis, because we hear more adven- 
titious sounds in many other conditions, notably bronchitis and bron- 
chiectasis, than in the average case of chronic phthisis. To be of 
significance the rales must be strictly localized over a limited area and 
persistent. It can be stated that, excepting in far-advanced cases, 
or the rare cases of chronic bronchitis complicating tuberculosis, and 
some forms of fibroid phthisis, the larger the area over which moist rales 
are heard, especially bilaterally, the less the likelihood of their being of 
tuberculous origin; the higher up in the chest they are exclusively audible, 
the more likely that they spell phthisis; and when heard exclusively at 
the bases or over the lower lobes the chances that they are tuberculous 
are rather scanty. Large bubbling rales, when heard over areas where 
there are no large bronchi, as in the upper third of the chest, are of 
greater significance than when heard over areas beneath which large 
bronchi are located. The latter may be caused by bronchitis or 


PROVOKED RALES 549 


bronchiectasis. When large bubbling rales are heard near the bell of 
the stethoscope, they are indications of phthisical excavation, because 
there are no large bronchi near the surface of the lung. ~ 

Sibilant and Sonorous Rales.—These are very often heard over 
tuberculous foci. In many incipient cases, especially in those with 
stationary or healing lesions, whistling and snoring rales are not uncom- 
monly localized over one apex, especially posteriorly. When not 
accompanied by crackles we may take them as an indication of healing, 
and that they are caused by the compression of the bronchioles by 
fibrous tissue which forms during the process of repair. Similarly, 
we hear sibilant and sonorous rales over a circumscribed area as the 
only reminders of an old and cured tuberculous process. In senile 
phthisis, sibilant and sonorous rales are often the only adventitious 
sounds. 

The asthmatic forms of phthisis, as well as those accompanied by, 
or implanted on, diffuse bronchitis and pulmonary emphysema, espe- 
cially in fibroid phthisis, often manifest themselves by sibilant and 
musical rales heard during inspiration and expiration. We hear all 
kinds of musical notes, snoring, cooing, whistling, grunting, groan- 
ing, whining, etc. ‘They may be heard alone while the respiratory 
murmur is feeble or inaudible, and then they may also be accompanied 
by all kinds of moist rales. Sibilant and sonorous rales or rhonchi are 
engendered by thick, viscid and tenacious secretions in the bronchi, 
or swelling or spasmodic contraction of these tubes. When heard 
exclusively over one of the upper lobes of a lung, they are almost 
pathognomonic of a tuberculous lesion. When audible all over both 
sides of the chest, the diagnosis of tuberculosis may not be an easy task 
and differentiation from chronic bronchitis, pulmonary emphysema, 
asthma, etc., can only be made after considering the signs revealed by 
percussion, as well as by the constitutional symptoms, and in some 
cases only the microscopic findings in the sputum can decide. When 
these sonorous and sibilant rales are heard unilaterally in the upper 
part of the chest they are easily diagnosed, as a rule. 

Provoked Rales.—In many cases of early phthisis, and also at times 
in those with advanced disease, no adventitious sounds are heard on 
ordinary, or even forced, breathing; but more or less vigorous cough 
brings out an explosion of rales. Some writers have spoken of these as 
“latent rales,’ which is an incongruous term. Bray! found that in 75 
per cent of cases of early phthisis, and in 30 per cent of those with 
moderately advanced disease, rales could be provoked by cough. We 
should not pronounce a patient free from adventitious sounds unless 
cough has been impotent in provoking them. 

The mechanism of production of these rales has been a disputed sub- 
ject. Some have suggested that they are produced by the separation of 
the collapsed walls of the alveoli and smaller bronchioles in and around 


1 Jour. Am. Med. Assn., 1916, 66, 788. 


300 AUSCULTATION OF THE CHEST IN PHTHISIS 


the diseased focus. Bray is not satisfied with this explanation and 
offers the following: Toward the end of expiration the glottis is volun- 
tarily closed and the intrapulmonary pressure is increased by powerful 
contraction of the expiratory muscles. This sudden increase in the 
intrapulmonary pressure separates the collapsed walls of the bron- 
chioles and alveoli and the atelectatic area. Once the patency of these 
structures is established, the rale is produced by means of the cough, 
which sets into vibration the pathological secretions contained within 
the bronchioles and alveoli. 

All kinds of rales may be provoked by cough. In early cases, some 
dry crackles may thus be brought out, or small, moist rales, and, at 
times, even showers of explosive rales may be provoked in cases in 
which no adventitious sounds were audible. In advanced cases large, 
moist, consonating rales may be brought out by cough when the 
bronchus leading to the cavity has been plugged, but the cough clears 
the passage, and permits the secretions to move with the air current. 
In others, sibilant or sonorous rales are thus provoked. The rales are 
usually heard during inspiration, but at times during both phases of the 
respiratory act. 

Of course, no attempt should be made to provoke rales during or 
after a pulmonary hemorrhage, for obvious reasons. 

Friction Sounds.—These are very often heard over phthisical 
chests. Over the apex they are heard best anteriorly above and 
beneath the clavicle, but here they are usually not very distinct because 
of the limitation of the motion of the lung in that region. Yet we 
sometimes perceive some grating. This is usually very difficult to 
differentiate from crepitation—all the criteria given in text-books 
are futile in some cases. At the lower parts of the thorax friction 
sounds are more common, especially in the axillary region. On rare 
occasions a pleuropericardial rub is heard not only during the respira- 
tory phases, but also synchronous with the heart-beat. It is an 
indication of dry pleurisy of the lingula or other parts of the pleura 
in contact with the pericardium. 

We distinguish friction sounds from rales by the fact that the 
former are heard superficially, right near the bell of the stethoscope; 
often they are increased by pressure of the stethoscope; they are 
uninfluenced by cough which usually increases the intensity of rales 
or entirely removes them; they are annulled when the breath is held. 
But the most important difference is that crepitant rales are heard 
during inspiration only, while friction sounds are audible during both 
phases of the respiratory act. However, in many cases it is quite 
difficult to state positively whether the adventitious sounds under 
consideration are of pulmonary or pleuritic origin. When found over 
an extensive area, especially posteriorly, or in the axillary region, 
frictions may be diagnosed by assuming that rales over such a large 
area would represent a very extensive pulmonary lesion with severe 
constitutional symptoms, while pleurisy may persist for years without 
impairing the general condition of the patient very much, 


SPURIOUS RALES 301 


Spurious Rales.—Rales of extrapulmonary origin are occasionally 
heard while auscultating chests, and attributed to tuberculous changes 
in the lungs. In persons suffering nasal obstruction we may hear 
various sounds resembling rales which disappear when the patient is 
made to breathe through the mouth. A frequent cause of extra- 
pulmonary rales is the falling back of the tongue when the patient 
makes strong efforts to breathe deeply, also after vigorous coughing 
the patient swallows and we believe that we hear rales in the chest. 

Other spurious rales, described by Peretz! and William Ewart? in 
England, Colonel G. E. Bushnell? and Hawes‘ in this country, are 
caused by muscular contractions, especially the trapezius, and on rais- 
ing and lowering the shoulders and arms. In persons who lift their 
shoulders when asked to breathe deeply these “rales” are often quite 
audible. French authors speak of them as craquements et frottements 
sous scapulaires, which can be heard very often over the upper part of 
‘the chest posteriorly. These muscle sounds were a potential source of 
error in 9.2 per cent of 250 cases examined by Hawes, while joint 
sounds were found in 22 per cent of cases. 

J. T. King,> examining over 22,000 soldiers for tuberculosis in the 
United States Army, looked especially for these joint sounds. He kept 
notes of 819 men as to the incidence of spurious rales in the upper part 
of the chest. In 33 cases, or 4 per cent, crepitations were audible at, 
or near, one or more joints. Most of these sounds emanated from the 
scapule, the costosternal and sternoclavicular articulations, and from 
the joints at the shoulder anteriorly. In 23 instances, certain crackles, 
usually rather loud and explosive, were heard during one or a few respir- 
ations over the apices, disappearing promptly during continued breath- 
ing. In 17 cases, or 2.07 per cent, there were found persistent apical 
clicks or crackles, of the type which had often proved confusing. Dur- 
ing the selective draft for the United States Army, several patients 
who consulted me after being rejected because of tuberculosis, were 
found to have these spurious rales in the chest. Some could not 
be convinced that they were not tuberculous, because many physicians 
told them that they have “rales” in the chest. 

The so-called atelectatic and marginal rales are even more often 
found and must be guarded against. They are mostly heard over 
the anterior and lower margins of the lungs and are probably caused 
by the unfolding of collapsed alveoli in individuals who breathe 
superficially and also by the peeling off of the diaphragm from the 
chest wall as the lung descends into the complemental space. Richard 
C. Cabot® found them in 61 per cent of normal chests and speaks of 
them as crepitant and subcrepitant varieties. They usually disappear 
after a few breaths, but at times they persist indefinitely. 


1 British Med. Jour., 1896, 1, 82. ZT bIds 191252, el 
3 Medical Record, 1912, 81, 101; 82, 1109. 

4 Boston Med. and Surg. Jour., 1914, 170, 153. 

5 Military Surgeon, 1918, 42, 60. 

6 Physical Diagnosis, New York, 1909, p. 163. 


o02 AUSCULTATION OF THE CHEST IN PHTHISIS 


Bushnell also described sounds originating in the sternum and its 
articulations, heard particularly at the second costal cartilage, which 
may lead to error, and I have been able to verify his findings in a 
large number of healthy persons, especially in muscular men. In some 
cases they resemble crepitation and occasionally even medium-sized 
moist rales and clicks, like the adventitious sounds of early phthisis. 
They can usually be differentiated from pulmonary rales by the fact 
that they are localized and heard loudest over the sternum and its 
articulations, but in doubtful cases, especially those showing a short 
note at one apex, they may lead to error. 

It is usually easy to differentiate these sounds from intrapulmonary 
rales, but at times they may prove confusing to the most expert. The 
crackles heard over the apex, originating in the neck muscles, are 
identified by their loud, explosive character, and by the fact that they 
are not influenced by cough. Moving of the head to one side or another 
may be effective in suppressing them. Bushnell and King suggest the 
following criteria for the identification of the joint crepitations: They 
are of a groaning or grating character and disappear when the patient 
folds his arms and grasps the opposite shoulder with his hands; by 
having him; while standing, bend the trunk forward to a horizontal 
position and allow the arms to hang limply downward; by having 
him grasp an-object at a level about as high as he can reach, and exert 
enough weight on his arms to fix the scapule apart. Crepitations from 
the lateral sternal articulations may often be eliminated by having the 
patient throw his shoulders as far back as possible. 

Voice Sounds.—Bronchophony adds little if anything to the infor- 
mation we gain by percussion and auscultation. It is generally heard 
over areas which are dull on percussion and show bronchial breathing. 
Moreover, it is necessary that the pulmonary consolidation should 
be superficial in order to produce distinct bronchophony while the 
breath sounds may be altered with moderately deep lesions. Of course, 
loud transmission of the voice suggests dense pulmonary consolidation 
through which a bronchus is passing, while decreased voice sounds 
indicate pleural effusions, thickened pleura, emphysema, or merely 
thick chest walls; in short, anything that diminishes the conductivity of 
the lung, and intervenes between the large bronchi and the surface. 
Even a plugged bronchus may diminish or abolish the voice sounds, 
which reappear after vigorous cough. 

Bronchophony is very loud in persons with thin chest walls, or who 
haye a deep voice; and, in general, in the interscapular space, especially 
in the right side, for obvious reasons. The various distinctions of 
bronchophony, pectoriloquy, ete., have no significance in the diagnosis 
of phthisis. | 

Whispered Voice.—Of greater importance is the auscultation of the 
whispered voice. In this it is really not the voice that is transmitted 
but the breath sounds, to which are added different reverberations 
from the oral, pharyngeal, and nasal cavities. My experience is in 


WHISPERED VOICE BIa)s) 


agreement with that of Sewall to the effect that in auscultation of the 
whispered voice we have an unrivalled means for the detection of 
minute changes in the pulmonary tissue. I have been able to outline 
consolidations and excavations of lung tissue by carefully studying 
the whispered voice, and other methods of diagnosis have merely 
confirmed the findings. Inasmuch as it is very easy to acquire, it 
ought to be more generally adapted in the routine study of phthisis 
in all its stages. 

We must, however, remember that the chest walls are also vibrating 
when the person whispers and especially when he talks, as has been 
shown by Sewall.!. He suggests that the mural vibrations should 
be damped by pressure with the stethoscope, and thus only the visceral 
vibrations will be brought to the auscultating ear. He shows that, in 
general, it may be said that with the intense congestion of the lungs or 
such tissue changes as occur in early phthisis, the voice takes on a 
more or less amphoric or tracheal character and it tends to become more 
distinct, prolonged, raised in pitch and nearer the ear, with pressure 
of the stethoscope on the surface of the chest. When the patient 
counts “one, two, three,” there is a tendency for the voice to linger 
with a bleating echo which is exaggerated by stethoscope pressure. 
This has often helped me in doubtful cases in which both percussion 
and auscultation were absolutely inadequate to justify a final opinion. 

Whispered pectoriloquy is also of immense value in patients with 
laryngeal involvement, or who have pleural pains and cannot breathe 
deeply, and especially in patients soon after a hemorrhage when we 
should hesitate in going through all the diagnostic maneuvers which 
may cause the bleeding to recur. Whispered pectoriloquy, bron- 
chophony and auscultation during ordinary breathing can give us 
sufficient information to form an opinion on the extent of the lesion. 

Over healthy lungs the whispered voice is audible in the upper third 
of the chest, especially on the right side, while in the lower parts it 
is hardly, or not at all, audible. An increase in the intensity is an 
indication of better sound conduction—consolidation or compression 
of pulmonary parenchyma, or even congestion, as has already been 
mentioned. It is therefore an early sign of phthisis. It must, how- 
ever, be borne in mind that it is heard over healed lesions and there- 
fore is not to be taken for a sign of activity of the process without 
confirmation by constitutional symptoms. 

Over air-filled cavities, pulmonary or pleural, we hear what Kuthy? 
calls “amphorophony’’—the transmission of the whispered voice with 
an amphoric or metallic echo. It is an indication that the cavity or 
the pneumothorax has smooth walls. In cases with cavities we can at 
times make out the extent of the excavation by auscultation of the 
whispered voice as well as by any other method. 


1 Jour. Am. Med. Assn., 1913, 60, 2027; Sewall and Childs: Arch. Intern. Med., 1912, 
10, 45. 
2 Die Prognosenstellung bei der Lungentuberkulose, Berlin, 1914, p. 302. 


23 


CHAPTER XVIL 
ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS. 


Soon after the introduction of the a-rays, great hopes were enter- 
tained that finally a means of visualizing the condition of the thoracic 
viscera and detecting any changes in the lungs, bronchi, and pleura 
had been obtained. “But after several years’ experience it was found 
that in tuberculosis roentgenography has its limitations, just as other 
diagnostic methods. On the one hand, it does not disclose infiltrations, 
the very early changes in phthisis; on the other hand, because it clearly 
shows caseated and calcified foci, revealing airless areas of lung tissue, 
it helps in establishing an anatomical diagnosis. Whether the changes 
discovered are tuberculous in character, and whether the lesion is 
active, must be ascertained by other clinical methods. For this reason, 
roentgenography, while a very important aid in diagnosis, cannot be 
relied on to the exclusion of other methods. It does not disclose 

catarrhal conditions nor does it reveal infiltrations. 

When properly used, roentgenography helps materially in discloses 
certain changes in the intrathoracic viscera which formerly escaped 
notice during the life of the patient. Especially is this true of deep- 
seated lesions, pleural adhesions, enlarged bronchial glands, localized 
and interlobar effusions, localized pneumothorax, small cavities in 
the lungs, the motion of the diaphragm, abscess and gangrene of the 
lung, ete. 

The condition of the lung and the changes at the site of the lesion 
in the average éase of early phthisis can be made out easily by auscul- 
tation and percussion. ‘The former even gives important indications 
as to the activity of the process discovered. But the a-rays complete 
the examination and often reveal deeper-lying changes in the chest 
which otherwise escape detection. Moreover, the practice of artificial 
pneumothorax, which has lately been applied with such striking success 
in proper cases, could not have gained general acceptance but for 
roentgenography. 

The technic of x-ray examination, especially the comparative value 
of the various apparatus employed, will not be discussed here. This 
is the province of specially trained technicians. But every physician 
handling tuberculous cases should be able to read an x-ray plate and 
not depend entirely on the specialist roentgenographer for interpretation 
of the findings. When interpreted in connection with the clinical symp- 
toms, with which the physician alone is acquainted, the x-rays yield the 
best results. 

Appearance of the Normal Chest.—The appearance in the normal 
chest should be known before attempting to decipher pathological 


Roentgenogram of a man with apparently healthy thoracic viscera. Dorsoventral positio 


Fie. 


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APPEARANCE OF THE NORMAL CHEST 309 


changes. It is, however, a fact that a normal chest, showing no signs 
suggestive of pathological conditions, is exceedingly rare. I have not 
yet seen one. Plate X shows plates from a chest of a man apparently 
free from pulmonary disease. 

While passing through the thorax, the rays are obstructed by the 
various tissues, according to their density, volume and constituent 
elements, and the result is that the denser tissues cast shadows on the 
screen or plate. The ribs cross the lung fields appearing as dark, 
sharply defined bands, their posterior parts are seen forming a con- 
cavity downward, while the anterior parts are convex downward. 
In normal healthy young persons the costal cartilages are not all visible. 





Fig. 81.—Structures making up the hilus shadow: R, second rib; W, second thoracic 
vertebra; V, arch of azygos vein; B, bronchus; LZ, bronchial lymphatic glands; A, aorta; 
P, pulmonary artery; O, esophagus; D, thoracic duct. (Doyen.) 


However, early ossification of these cartilages is consistent with 
healthy lungs in many cases. The clavicles produce a distinct shadow, 
running horizontally outward and _ slightly downward. In some 
persons the clavicles overlap the first ribs and thus obscure the lung 
apex. ‘The scapule also are visible as more or less distinct triangular 
shadows. 

The densest shadow seen is that of the heart and great vessels in 
the middle and to the left, and the diaphragm beneath. Because 
it permits the rays to pass with less resistance than any other organ 
in the chest, the lung gives a dark image on the negative; the heart, 
the large vessels, the diaphragm and the liver, because of their density 


306 ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


and blood content, obstruct the rays and produce light areas on the 
plate. The most translucent parts of the healthy viscera are the 
healthy lungs; when they are collapsed by air in the pleura, as in 
pneumothorax, the space is even brighter. In healthy persons, when 
the patient takes a deep inspiration, the lungs brighten up. But the 
brightness of the lung tissue is not absolute. There is seen a delicate, 
at times even a more or less coarse, arborization, as of a network, 
passing from the roots of the lung to the periphery. At the roots it 
is caused by the greater density of the tissues, but in most persons 
also by the deposition of carbon particles, which may be found in 
nearly every individual over fifteen years of age. When the shadow 
at that point is abnormally accentuated, it may be an indication of 
enlargement or calcification of the glands, and in children it points 
to tuberculous tracheobronchial adenopathy. Often we note in this 
region small, sharply defined, oval opacities which represent optical 
sections of bloodvessels. 

It is, however, difficult or impossible to evaluate every shadow or 
opacity because by their passage through the chest the rays are 
obstructed by the various parts constituting the viscera, thus pro- 
ducing superimposed shadows. Carefully prepared stereoscopic pic- 
tures may enable us to distinguish these superimposed shadows in 
perspective, but they are after all not much superior to a good roent- 
genogram taken by instantaneous exposure. 

The Hilus Shadow.—The shadows seen at both sides of the heart 
are very frequently a source of confusion in diagnosis. As will be seen 
from Fig. 81, they are due to the density of the tissues composing the 
bronchi and the lar ge vessels, which are seen either in transverse, or in 
optical section, combined with the opacities produced by the regional 
lymphatic glands and connective tissue, none of which can be differ- 
entiated on the screen or plate. While in some cases circumscribed 
opacities, or spots, represent calcified glands or nodules, in others they 
are produced by deposits of dust in the peribronchial ly mphatic tissues 
which are very frequent in adults, and even in children in cities they 
are not uncommon. But in many cases simple engorgement of these 
tissues with blood is apt to give a shadow in that region. In fact, 
during attacks of measles or whooping-cough the glands in the chest 
have been found visible in roentgenographic plates, and the same is often 
the case in acute affections of the respiratory tract in children or 
adults. 

It is thus clear that many conditions other than tuberculosis of 
the tracheobronchial glands may cause shadows or opacities in the 
hilus region. Moreover, even when these opacities represent anthra- 
cotic or ee eous glands, the roentgenogram alone gives us no clue as 
to the activity of the process, which is after all the main problem in 
clinical diagnosis. In children it is hazardous to diagnosticate tracheo- 
bronchial adenopathy because of these opacities when the clinical 
picture is not in agreement. 


FLUOROSCOPY 357 


To the right side of the heart the hilus shadow is more extensive 
than to the left because in the latter location the heart shadow obscures 
the hilus structures. In many cases we see strands passing from the 
hilus to the periphery, or the diaphragm. It is the consensus of opinion 
that they are produced by bloodvessels, and occasionally by bronchi 
which at times appear in optical section. 





Fic. 82.—Diagrammatic representation of the location of the thoracic glands based 
on numerous observations of roentgenograms compared with anatomical findings. Only 
those at the roots of the lungs are represented in black, while those that are covered by 
the pulmonary artery and the roots of the bronchi and mediastinum are left out. 1, para- 
tracheal gland; 2, tracheobronchial gland at the aorta; 3, bronchopulmonary lymphatic 
glands at the hilum on both sides. (Assmann.) 


Fluoroscopy.—In the vast majority of cases of tuberculosis, and 
in suspects, a fluoroscopic examination is sufficient for diagnostic pur- 
poses; in the few cases in which a plate is desirable, fluoroscopy is not 
to be neglected, because it gives us information which the plate does 
not. Fluoroscopy is to be preferred in many cases because it shows the 
motion of the parietes of the chest, of the diaphragm, and of the 
pulmonary apices, etc. The room in which fluoroscopy is done must 
be totally dark, and inasmuch as this is very difficult to attain in the 
average physician’s office, it is best done in the evening. 

The following points are to be looked for on the fluoroscopic screen 
when examining a chest: The ribs; the median shadow; the dia- 
phragm; the hilusshadow; the space above the clavicle are to be carefully 
studied. 

In healthy and well-formed individuals the ribs are seen sym- 
metrically placed on both sides, moving with each respiratory act. 
Unilateral limitation of motion of the ribs is suggestive of unilateral 
disease, and phthisis is to be thought of in this connection. When we 
find the ribs on both sides unduly horizontal we should look for pul- 
monary emphysema; when the horizontal setting is unilateral, while 


358 ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


the lung markings are absent, pneumothorax is to be suspected. Nor- 
mally, especially in young subjects, the costal cartilages are not dis- 
tinctly visible on the screen. The ribs are sharply cut off (see Fig. 2, 
Plate X). In older persons they are usually visible, owing to ossifica- 
tion which takes place with advancing age. In tuberculous patients 
ossification of the costal cartilages, especially the first (Fig. 1, Plate 
XVID), is very frequently seen on the roentgenogram. As was already 
stated, Freund considers this a predisposing factor to phthisis because 
of the stenosis of the upper aperture of the thorax, which it is apt to 
cause. In some cases of phthisis all the costal cartilages are calcified, 
and when looking at a patient’s chest in the fluoroscope, this point 
should not be neglected. But it must be mentioned that it is not an 
infallible sign of phthisis. It may be found in persons who are not 
sick, while I have repeatedly observed cases of advanced phthisis in 
which the costal cartilages were hardly visible. 

Within the thoracic cavity the deep shadow representing the medias- 
tinal organs, the heart, aorta, pulmonary artery, vena cava, as well 
as the sternum and the vertebral column, is to be carefully examined. 
It is triangular in shape, the base extending markedly to the left of the 
sternum. The middle third of its right border represents the superior 
vena cava: when bulging out, the lower third represents the right 
auricle. The left border is made up of three successive convexities: 
The first is produced by the arch of the aorta; the middle, the pul- 
monary artery and the left auricular appendix; while the lower is the 
left ventricle of the heart. All or any of these convexities are seen, 
in many cases, to throb rhythmically; at times the succession of the 
beats of the ventricle and those of the pulmonary artery may be seen 
very clearly. In phthisis the heart is, as a rule, smaller than normal. 

The hilus shadow, on both sides of the median shadow, should be 
carefully studied. It is best seen in the right side because in the left 
it is in part covered by the heart. As was already stated, its signifi- 
cance is very frequently overestimated by roentgenologists. In healthy 
individuals it represents primarily the bloodvessels, the bronchi, the 
bronchial glands, and connective tissue which is abundant in that 
region. It is the consensus of opinion that this shadow merely indi- 
cates the absence of air and gives no clue as to each individual structure 
which enter into its make up. When the thoracic glands are enlarged 
or calcified, the hilus shadow appears larger and more accentuated. 
This point is discussed elsewhere in detail. 

The lungs are seen within the thoracic cage as two triangular bright 
fields; the upper part is separated from the rest by the shadow of the 
clavicle above which the lung apex can be inspected. The base is 
delimited by the diaphragm, which moves with each respiratory act, 
being raised during expiration and lowered during inspiration. 

The apices are carefully inspected, and the translucency of the 
lungs in these regions inquired into. Theoretically, it should be 
of equal intensity on both sides, but such perfection is only rarely 


FLUOROSCOPY 309 


encountered, even in healthy persons. Usually, owing to thickness of 
the muscles, scoliosis, ete., one side is somewhat darker. But this is 
best studied on the roentgenographic plate. With the fluoroscope we 
look for the “cough phenomenon,” first described by Kreuzfuchs.’ 
This author noted that in healthy individuals the translucency of the 
apices varies according to various conditions, especially the form of the 
chest. Deep respiratory efforts may clear up any shadow in healthy 
lungs. During cough the apices brighten up even when they are other- 
wise quite dark, excepting when there is diseased tissue in that region 
and the affected apex remains dark even during cough. 

But this is not a very reliable sign. Jordan? says: “Failure of the 
apex to light up is difficult to make out with certainty; there are 
endless fallacies due to the position of the z-ray tube, the thickness 
of the pectoral muscles of the patient, the ‘lie’ of the ribs and clavicle, 
etc., and at best it is almost impossible to reproduce this ‘failure’ on 
a photographic plate with any certainty. I am quite sure that we 
should diagnose pulmonary tuberculosis in a large number of healthy 
subjects if we are to rely on this sign.”’ 

This view is shared by many, but it appears that Jordan is mistaken 
in his statement to the effect that the cough phenomenon cannot be 
reproduced on a roentgenographic plate. As will be noted on Plate 
XII, F. Holst? has succeeded in reproducing this phenomenon very 
clearly. Moreover, this author has also shown that during cough there 
is an alteration in the lateral limits of the pulmonary apices, they be- 
come wider while the trachea becomes narrower, sometimes as much 
as lem. In normal individuals this phenomenon is observed on both 
sides to the same degree, while in case one apex is altered by tuberculous 
changes, it fails to brighten up, and remains narrow and darker during 
cough. Of course, this phenomenon is best studied on the screen, 
and only exceptionally may it be reproduced on a roentgenographic 
plate. We must, however, guard against mistaking the apparent 
changes in the brightness of the apices during cough caused by the 
separation of the ribs and widening of the intercostal spaces. It has 
been of immense service to me in many Cases. 

With the aid of fluoroscopy we also ascertain the size and position 
of the heart. In phthisis this organ is, as a rule, smaller than normal. 
In fact, when I find a large heart in a dubious case I hesitate before 
making a diagnosis of phthisis. In phthisis it is also very often ver- 
tical; it may be “hanging,” cardioptosis, and in more advanced cases 
frequently displaced toward the affected side. 

After the apices, the diaphragm should claim our attention. The 
mobility of this muscle has been found defective on the affected side 
in many cases of phthisis; according to F. H. Williams,’ in the very 


1 Miinchen. med. Wchnschr., 1912, 59, 80. 

2 Lancet, 1914, 1, 963. 

3 Miinchen. med. Wehnschr., 1912, 59, 1659. 
4 Am. Jour. Med. Sci., 1897, 114, 655. 


360 ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


incipient stage. The motion of one-half of the diaphragm may not 
only be delayed when there is a pulmonary lesion, but it is at times 
seen to be “jerky,” or “stammering,” as Harold Mowat says. In 
some healthy persons the mobility of the diaphragm is very limited, 
while in most the breathing excursion is from three-fourths to one 
inch, and during forced respiration it may even move more than two 
inches, the left half of the muscle more than the right. When both 
sides are stationary it may indicate emphysema, or nothing at all, 
but when one side moves while the other is immobile or its excursion 
is relatively limited, we should suspect tuberculosis. Various explana- 
tions have been given for this phenomenon. Some have attributed it 
to diminished power of retraction of the lung, others to implication 
of the terminal branches of the vagus, or of the phrenic nerve in apical 
pleural thickenings, etc. In advanced cases limitation of motion may 
be due to pleural adhesions. It must, however, be emphasized that in 
itself defective movement of the diaphragm may be found in healthy 
individuals. If unilateral it may be due to paresis of that muscle, or to 
an old basal pleurisy producing adhesions which hinder its excursion. 
In persons with big abdomens, the breathing is usually purely thoracic, 
and the diaphragm is immobile. 

Extensive expertence has shown limitation of motion on the affected 
side of the diaphragm in only a few cases of incipient phthisis. Indeed, 
we often see advanced cases in which both sides of the diaphragm 
are freely and equally mobile. On the other hand, limitation is found 
in non-tuberculous cases owing to adhesions remaining after previous 
attacks of pleurisy the individual being quite healthy at the time. 
In advanced cases this phenomenon has to be considered in connection 
with the feasibility of artificial pneumothorax, but, as will be shown 
later on, it is not absolutely reliable. 

At the outer extremities of the diaphragm are the costodiaphragmatic 
sinuses. 'They should be examined carefully in every case, and both 
sides should be compared. The lower angle of the sinus should be 
long and sharp; during inspiration it enlarges and brightens up; it 
contracts and loses its brilliancy to some degree during expiration. 
Any diminution in its size, or obtuseness of its apex, or its complete 
obliteration, indicates a pathological process of the pleura or lung. 
The two sides should then be compared, but it must be borne in mind 
that in the right side the liver makes it somewhat smaller, while in 
the left side the air bubble of the stomach may alter it to some degree. 
The angle formed by the heart and the liver, the cardiohepatic angle, 
often appears obtuse, or obliterated in tuberculosis, especially pleurisy, 
or thickened pleura. The dome of the diaphragm is also changed by 
a thickened pleura; it is no more smooth, but shows marked elevation 
of the curve during inspiration; in others, we note a series of small 
irregularities in the contour; in still others, bands of connective tissue 
are seen passing from the diaphragm to the lung. 


Pere AL 


inne, 1! 





Roentgenogram of a woman with apparently healthy thoracic viscera. 


ities, 24 




















Roentgenogram of the chest of a child Roentgenogram of a child nine years old, 
eight years old. Though no symptoms or suggestive of enlarged hilus glands. The 
signs of tracheobronchial adenopathy could symptoms and signs of this disease were, 
be found clinically, the roentgenogram however, lacking. On a level with the 
shows shadows suggestive of such a condi- second rib an opacity suggestive of a 


tion. calcified gland can be seen. 


PLATE All 


Gat Fic, 3 





Lunggapex during ordinary breathing. Apex during ordinary breathing. 


Fie, 2 Fiq. 4 














The same apex while patient is cough- The same apex while patient is coughing, 
ing, and showing a narrowing of the showing narrowing of the trachea and 
trachea, widening, and lightening up of lightening up of the area of the lung. (F. 
the apices, especially the right. (F. Holst.) 

Holst.) 


The **‘Cough Phenomenon,” 


RUA eA El 


iivek il 











Roentgenogram of a case of abortive 
tuberculosis. Though suggestive of an ex- 
tensive lesion in the left apex, the physical 
signs, as well as the course of the disease, 
showed that the activity of the process was 
benign. The patient recovered within 
three months. 


Fie. 3 





Slight infiltration of the right apex. 
Marked increase in lymphatic tissue in 
both hilus regions. 


Wiley, & 











Roentgenogram of the apices in acase of 
incipient phthisis. No definite changes 
are visible, though physical exploration 
revealed a distinct lesion in the left apex, 
and the constitutional symptoms were 
clearly those of phthisis. 


Fie. 4 





Partial consolidation of both apices, 
large cavity in left apex and thickened 
interlobar fissure. Dilatation of bronchi of 
lower lobe of left lung. Heart displaced to 
the left. 


Riga ely 


Idiget, a Fig. 2 


























U =| = 
Fibroid changes in right apex, which Fibrocaseous lesion in right apex. Peri- 
some call an “incipient lesion.’’ Hilus bronchial fibrosis visible at each hilus. 
shadow strongly marked. Peribronchial 
fibrosis. 
Fia. 3 Fic. 4 














Tuberculous lesion of the fibroid type Miliary tuberculosis of the upper lobe 
in the right upper lobe. Sputum positive. of the right lung. Substernal thyroid in 
Substernal thyroid protruding into the the left side. 


upper third of the left chest. 


PLATE XV 


Fig. 1 





Fibrocaseous lesion in right apex. Peri- 
bronchial infiltrations and calcified glands 
at the hilus on both sides. 


Hie. 3 











Large cavity surrounded by a dense 
fibrous wall in upper part of right lung. 
Enlarged glands in right hilus region. 
Lower half emphysematous. Left lung 
shows moderate infiltration beneath the 
clavicle and enlarged hilus glands. Drop 
heart. 














| 


Very dense infiltration. of right upper 
lobe and large cavity below the clavicle 
limited below by the thickened interlobar 
fissure. Marked peribronchial infiltrations. 
The hilus region on both sides shows 
old fibroid and calcified glands. 





Hie. 4 











Bilateral tuberculous infiltration of both 
lungs. Dense hilus region due to ecalcifica- 
tion of glands. Several small cavities 
in right lung. Adhesions of diaphragm. 
Trachea markedly pulled over to the right. 
Stomach visible at left base. 





PLA TEx Va 


Fic. 1 





Moderate caseation of both apices. 
Coarse infiltration of lower half of left lung 
with thickened pleura. Heart pulled over 
to the left and downward. Emphysema of 
right lung. Diaphragm in right side 
shows a bulging due to adhesions. 


Fie. 3 














_Chronic cavitary phthisis in a child 
eight years of age, with displacement of 
the heart to the left. 











Diffuse caseation of upper third of left 
lung. The rest presents a dense homo- 
geneous shadow caused by consolidation 
of pulmonary parenchyma as well as 
thickened pleura. Right lung emphyse- 
matous and several calcified glands are 
seen at the hilus. 


Kia. 4 











Anthracosis and fibroid _ phthisis. 
Diffuse nodular infiltration of both lungs 
with multiple cavitation. ‘‘Honeycomb” 
appearance. 


PIA He XV ET 


Hie: 1 





Cavity in upper lobe of right lung filled Same patient as in Fig. 1. Secretions 
with secretions. emptied from the cavity by expectoration. 
Fig. 3 





Large cavity in upper lobe of the right Partial pneumothorax of upper half of 
Jung with fluid level. Partial pneumo- left lung with fluid level. Emphysema of 
thorax which has not been effective in right lung. 


compressing the cavity. 


PLATE XVIII 


Fig. 1 Fig. 2 











Dense consolidation of lower half of right Diffuse caseation of both lung apices. 
lung with thickened pleura. Large cavity Round cavity, surrounded by a dense 
in left lung occupying apex on a level fibrous capsule, under the right third inter- 


with first two interspaces. Drop heart. space in mammillary line. Irregularity 
of the diaphragm due to adhesions. 


itiqes, 33 Hig. 4 





Large, oval-shaped cavity in right upper Vertical heart. Multiple cavitation in 
lobe. Lymphatic tissue at hilus increased. right upper lobe, ‘‘honeycombed.”’ Lower 
“Annular shadow” in middle portion of part emphysematous. Small cavities in 
left lung at third interspace. Heart left upper lobe. Marked hilus changes. 


dropped; pleuropericardial adhesions. 


ROENTGENOGRAPHY 361 


Roentgenography.—Of great value in all stages of phthisis, especially 
in dubious early cases, and in those in which a permanent record is 
desired, is roentgenography. When properly taken and developed, the 
plate may be studied at leisure and slight alterations, which are not 
visible on the fluoroscopic screen, may be detected. 

In evaluating the roentgenographic findings we must bear in mind the 
following points: Small infiltrations do not show any definite and 
clear-cut signs on the plate; at any rate, the shadow they cast is not 
pathognomonic. Cohn! inserted tuberculous tissue into healthy lungs 
of cadavers, of which he took roentgenograms and found that 1 ce of 
diseased tissue is not visible on the plate. Ziegler and Krause? have 
investigated the problem and found that pieces of tissue less bulky 
than 4 ce are not visible on the roentgenogram, and that, on the w hole, 
small areas of infiltration are only visible when they are located near 
the surface of the lung. Experimental investigations of Joseph Walsh, 
James W. Wood and J.C. Thompson confirmed the above findings.’ 
In other words, small infiltrations, when centrally located, are screened 
by normal pulmonary tissue, and may escape detection. When the lesion 
has caseated it casts a more or less dense shadow. But then the case is 
no more incipient. 

In many cases we find that the affected apex is darker than its mate 
on the opposite side. In others, the affected area has the appearance 
of “ground glass.” But even this does not invariably imply an active 
lesion. Indeed, it may be put down as a general rule that, in suspicious 
cases showing no constitutional symptoms, the darker the apex, the 
less likely che probability of its being a sign of active incipient tuber- 
culosis. It may be rev ealing an old and healed lesion. Walsh and 
his coworkers, comparing lungs removed, with roentgenographic 
plates taken during life found that the greater the amount of fibrous 
tissue, the greater the density of the shadow. I have been impressed 
with the following fact: A considerable proportion of apparently 
healthy people have one apex, usually the right, darker, due to various 
causes. In many it represents healed tuberculous lesions which are no 
longer active, nor serious. When in these individuals there occurs 
a new tuberculous lesion in the opposite apex, which is not uncommon, 
it is responsible for the constitutional symptoms calling for a roentgeno- 
graphic examination. The report from the roentgenographer may state 
that the lesion is located in the right side, while the physical signs 
show conclusively that the active lesion is in the left, or the reverse. 

The divergence of findings on physical examination and roentgen- 
ography is best seen in far-advanced cases of phthisis in which a new 
lesion occurs in the hitherto unaffected apex. The plate does not show 
it distinctly until caseation has taken place, while physical exploration 
reveals it clearly. I have had this incontrovertible proof of the inade- 


1 Ztschr. f. Tuberkulose, 1911, 17, 217. 
2 Roentgenatlas der Lungentuberkulose, W ere 1910. 
3 Tr. Nat. Tuberc. Assn:, 1919, 15, 69. 


362 ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


quacy of roentgenography in incipient lesions repeatedly. Joseph 
Walsh also found that “physical signs have frequently brought out 
lesions and extensions invisible on the 2-ray, while the latter have 
shown only rare ones not found by the former.” 

For these reasons we should not conclude merely on finding opacities 
in one apex that we are dealing with a case of active incipient phthisis. 
When found in connection with constitutional symptoms and signs on 
physical exploration these opacities are of diagnostic value. Nor should 
we conclude in the presence of constitutional symptoms and local signs 
suggestive of phthisis, but negative roentgenographic findings, that a 
case is not tuberculous. Such a case requires further observation, 
despite the negative x-ray findings. I do not hesitate to make a 
diagnosis of pulmonary tuberculosis under such circumstances when 
clinical evidence warrants it. 

After the apex we carefully examine the condition of the roots of 
the lungs, the hilus, with a view of ascertaining the presence of enlarged 
caseated or calcified glands or peribronchial infiltrations in that 
region. The shadows and mottlings observable at these points have 
been discussed. At first there was a tendency to consider all abnor- 
malities as evidences of enlarged glands, and a diagnosis of tuber- 
culosis, or tuberculous adenopathy, was made on this evidence alone. 
But experience has shown conclusively that this shadow may be 
caused by any congestive condition and especially by fibrosis due to 
various causes of the glands, bronchi and lungs, and it is not pathog- 
nomonic of phthisis. There is hardly an adult living in a city, or 
working at a dusty trade, who has no peribronchial thickening, en- 
larged, or calcified, glands at the hilus of the lungs. It was also 
found by Cohn, Dunham, Boardman, Wolman, Bibb and Gilliland, 
and others, that except in cases with calcified glands, these shadows 
are caused by blood in the vessels ofthethorax. Bloodisknowntoabsorb 
the a-rays more readily than infiltrated soft tissue or sputum. Experi- 
mental injection of the arteries in the lung has been found to intensify 
the shadow, and in human beings injection of the vessels with substances 
giving a strong shadow produces pictures which are exactly like those 
of normal lung markings. But even this interpretation has recently 
been challenged by Joseph Walsh and coworkers. He found experi- 
mentally that an artery the size and thickness of the carotid casts so 
slight a shadow even when filled with blood that it is likely the blood- 
vessels per se have little or nothing to do with the hilus shadow, or 
normal lung detail. It is his opinion that the hilus shows up, not on 
account of specific structures, but merely on account of lack of air 
content. 

These facts explain many of the thickenings and strands noted on 
chest plates, running from the hilus to the periphery of the lungs. 
In some cases they are due to bronchitis with congestion; in others, 
the mottling is due to strands of connective tissue, or calcified glands 
which though tuberculous in origin, still are harmless and of no clinical 


SOURCES OF ERROR 363 


importance. Sewall and Childs report the case of a presumably 
non-tuberculous stone-cutter furnishing a roentgenogram in which, 
except for the relatively moderate involvement of the apices, the 
mineral deposits occasioned opacities resembling the densest tuber- 
culous structure. I have often had the same experience with workers 
at dusty trades. The criterion given by some authors for distinguish- 
ing inactive consolidations and calcified glands from shadows repre- 
senting active lesions by the fact that the latter appear “wooly,” 
does not hold in many cases. Any structure out of focus appears 
diffuse—‘ wooly”’; even instantaneously taken plates are not free 
from this source of error. In most cases when we find mottling, 
especially surrounding extensive lesions we are justified in considering 
them tubercles and an extension of the process; but we have seen many 
cases in which the plate showed extensively scattered tubercles, “a 
thick snowstorm,” yet at the autopsy no miliary tuberculosis was 
found. Miliary carcinomatosis of the lung gives a similar picture on 
the plate. I have had several patients with plates taken by radiog- 
raphers which showed these scattered tubercles, thus inducing these 
x-ray specialists to make diagnoses of miliary tuberculosis. Yet these 
patients walked into my office for examination, were found afebrile, 
and the subsequent course indicated that they had no real miliary 
tuberculosis. “The interpretation of less dense and more diffuse 
opacities is chiefly guesswork,” say Sewall and Childs.!. “They 
usually represent either pathological lymph nodes or bloodvessels in 
more or less optical section.” 

Sources of Error.—The analysis of these shadows and mottlings 
admits of so many interpretations that they are of doubtful utility 
in most incipient cases. The “ ground-glass” appearance of an apex 
is found in plates taken from healthy individuals and no symptoms 
indicating caseation of lung tissue can be found on prolonged clinical 
observation. A shadow in the apical region, when not the result of 
scoliosis, shows that there is some airless tissue in that location. 
But we are not justified in invariably assuming that it was caused by 
a tuberculous infiltration; or even if so, that the lesion is active. Ziegler 
and Krause, Dehn, Arnsperger, Assmann, and others have found that 
calcified and caseated tissue, and even fluid, anthracotic and calcified 
lymph glands, and most commonly connective tissue produce the same 
roentgenographic shadows. I have seen a large empyema failing to 
disclose itself on an x-ray plate. 

There is no more justification for placing an individual, one of whose 
apices casts a shadow on a plate, under prolonged and costly treatment 
than there vs for the treatment of one for mitral insufficiency merely 
because a systolic murmur vs audible at the cardiac apex. In both cases 
the clinical symptoms decide whether the person is sick and in need of 
treatment. 





1 Arch. Int. Med., 1912, 10, 45. 


364 ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


Because we are looking, in incipient cases, for small areas of recent 
infiltration, it is clear that we cannot rely on roentgenography alone for 
the diagnosis of early phthisis. The roentgenographic picture gives 
the history of the thoracic viscera throughout the life of their owner. 
Any pathological change which may have occurred at any time may 
have left traces behind which are likely to cast shadows or cause 
opacities on the plate. For this reason, in incipient or dubious cases, 
the roentgenographic findings are to be taken only in connection with 
constitutional symptoms and physical exploration of the chest. If the 
latter are negative, the case is to be considered non-tuberculous, no 
matter what the roentgenographic plate shows. 

It is thus clear that in the diagnosis of incipient phthisis the x-rays 
are not of the value which some authors have attributed to them. 
Early tuberculous lesions, slightly enlarged bronchial glands, unless 
caseated or calcified, as well as mucous secretions, usually permit 
the rays to pass through without casting any shadows on the plate. 
Optical sections of bloodvessels, due to any condition that may cause 
vascular engorgement, may show opacities on the plate simulating 
the characteristics of tuberculous lesions and may lead to error. 

What is of most importance in obscure lesions is not so much their 
causation but their activity. A healed tuberculous lesion in an apex 
is not incompatible with excellent health, as has been repeatedly 
emphasized. But the cicatrix produced by the healing process pro- 
duces a shadow on the roentgenogram as well as, and often more 
striking than, an active lesion. 

Roentgenography may be of great assistance in attempts at localiza- 
tion of a lesion, though smaller tuberculous foci may often be discovered 
with the orthodox clinical methods of diagnosis, and the determination 
of the activity of an apical process can only be accomplished by careful 
observation of the case, paying special attention to the constitutional 
symptoms, such as the temperature, the pulse, cough, expectoration, 
and the physical signs. “With our present ability to produce and 
interpret x-ray pictures,” say Sewall and Childs, “it must be admitted 
that a judgment founded on clinical history combined with physical 
signs may lead to a strong suspicion of tuberculous infection long before 
any signs of actual tissue changes, except those involving bronchial 
glands, appear on the x-ray negative.’ Wolman,! who has worked 
with the stereograph, arrives at a similar conclusion. He says: “In 
the great bulk of cases the stereograph tells us no more than a careful 
clinical examination, yet in a fair number of cases, and those among 
the most interesting and puzzling, it gives additional information. 
But we must add the caution that a careful history is indispensable, 
since not even the stereograph can tell an active from a healed lesion.” 
Likewise Joseph Walsh says, “Advanced tuberculosis with massive 
fibrosis or caseation, numerous tubercles, or large cavitation can 


1 Johns Hopkins Hosp. Bull., 1911, 22, 236. 


ROENTGENOGRAPHY IN ADVANCED STAGES OF PHTHISIS 365 


usually be diagnosed by the a-ray, though still more accurately by 
physical signs. The best results are achieved by careful physical 
diagnosis compared with the v-ray plate and, if differences are found, 
submission of these to physical examination before conclusion is 
reached. Physical signs have frequently brought out lesions and ex- 
tensions invisible on the a-ray; while the latter have shown only rarely 
ones not found by the former.” 

When my findings on physical exploration of the chest disagree 
with the roentgenographic shadows and interpretation, I place more 
reliance on the purely clinical methods, and quite extensive experience, 
with many autopsies have taught me that careful and competent 
physical diagnosis is more reliable in doubtful cases than roentgen- 
ography. 

Roentgenography in Advanced Stages of Phthisis.—In my experience 
roentgenography has been of greater utility in the diagnosis of advanced 
disease than in early or dubious cases. However, only rarely we find 
that the z-ray plate reveals more extensive involvement than the 
findings on physical exploration of the chest. In cases in which the 
question of artificial pneumothorax is considered, roentgenography 
offers invaluable assistance. Very often pleural effusions, especially 
the localized or interlobar varieties; pneumothorax and pleural adhe- 
sions, are discovered, though they have escaped detection by routine 
methods. The same is particularly true of localized pneumothorax. 

The roentgenographic picture of advanced phthisis is variegated, 
depending on the changes in the lungs and pleura. The intensity of 
the shadows cast by the lesions depends on their nature and density. 
Caseated and calcified areas cast dense shadows, while proliferation 
of tissue, especially when it is also congested, or fibrosis, is also clearly 
detected. Old, indurated areas are usually more or less sharply demar- 
cated from the surrounding tissues, while with new, active infiltrations 
the shadow merges by degrees with the surrounding air-containing 
lung tissue. Thick pleura is discovered by a dense, uniform shadow, 
and all connective-tissue formations reveal themselves in the same 
manner. More often than by physical exploration, cavities disclose 
themselves by showing limited areas lacking in lung markings and 
surrounded by thick shadows (Plates XV, XVII). They may often be 
seen moving during inspiration and expiration when examined with the 
fluoroscopic screen. But when a cavity is filled with secretions it is 
again airless and casts the shadow of the surrounding tissues, and a 
very much thickened pleura may cover up a cavity. The difference 
in appearance of a cavity when filled with secretions, and then when 
the secretions have been brought out by expectoration is well shown on 
Plate XVII. A cavity may also be screened by the surrounding 
healthy lung tissue. Thus, we often fail to find it with the v-rays, 
while physical exploration reveals it easily. Sampson, Heise, and 
Brown! have recently shown that in many cases the annular or ring- 


1 American Review of Tuberculosis, 1919, 2, 664, 


366 ROENTGENOGRAPHY IN THE DIAGNOSIS OF PHTHISIS 


like shadows seen often in almost normal or mildly infiltrated lung 
fields are no indications of intrapulmonary cavities, as has been 
supposed by many, but altogether localized, usually interlobar pneu- 
mothorax. The writer has not been able to confirm these findings. 
In several cases these annular shadows were clearly marked on the 
roentgenograms, yet neither cavities nor interlobar pneumothorax 
were found. 

The differentiation between thick pleura and pleural effusions is 
very difficult in most cases; in many impossible, if we rely on roentgen- 
ography alone. The following rule may be of assistance in some cases: 
When the signs found by percussion show a more extensive lesion than 
the roentgenogram shows, then it is the thickened pleura which pro- 
duces the dulness. Conversely, when the signs obtained by percussion 
indicate a lesion of slighter extent than the roentgenogram reveals, 
there is a central parenchymatous lesion of very serious import. 

The condition of the pleura may be studied on the plate. Fibrinous 
pleurisy is not shown at all, and very often quite a thick pleura, easily 
discovered by physical diagnosis is not seen on the plate. I have seen 
at an autopsy quite a thick pleura, about 1 em. in thickness, which 
gave no indication of its presence on the roentgenographic plate. 
But an effusion reveals itself clearly as an intense homogeneous shadow 
on the plate. Its upper level is not clearly demarcated from the lung 
above, and in the fluoroscope it may be seen moving somewhat with 
the respiratory movements. When the quantity of fluid is small, it 
may escape detection when sinking down in the diaphragm. In hydro- 
pneumothorax it is important that the exposure should be made with 
the patient in the erect posture, because when lying down small quan- 
tities of fluid spread in a thin layer and may escape detection. In 
hydropneumothorax the upper layer of the fluid forms a sharp line, 
while in pleurisy with effusion the upper level is usually not so sharp, 
but gradually merges with the lung tissue above it. The fact that in 
the latter case the level does not shift with motion of the patient’s 
chest shows that it is not a hydropneumothorax; in the latter case it 
does shift (see Plate XXIII). 

The displacements of the mediastinum caused by pleural effusion 
are best made out with the x-rays; but it is impossible to distinguish 
between fluid and the liver in right-sided effusions. Dislocation of the 
trachea and larynx may often be discovered on the plate (Plate XV). 


CHA PLE Rex LEE 
THE CLINICAL FORMS OF PHTHISIS. 


POLYMORPHISM OF THE CLINICAL PHENOMENA OF 
PHTHISIS. 


LAENNEC showed clearly the unity of the elemental pathological 
changes occurring in phthisis, and Koch, discovering the tubercle 
bacillus, proved it etiologically. But all attempts to impose this unity 
on the clinical manifestations of tuberculous diseases of the lungs have 
failed dismally. In pathology, particularly in clinical medicine, unity 
of causation does not always indicate unity of effect. Especially is this 
true of a polymorphous disease, as pulmonary phthisis. 

A study of the morbid anatomy of phthisis shows great polymor- 
phism—there are hardly two cases showing the same changes in 
structure. There are cases in which the lesions are purely proliferative, 
characterized by the formation of tubercles, as is the case with acute 
miliary tuberculosis; in others they are mainly exudative, as in chronic 
phthisis. But in the latter the difference in the intensity of the pro- 
ductive inflammation, which tends to limit the morbid process; and 
the process of necrosis, which tends to extend it, produce a diversity 
of lesions which have important bearings on the clinical picture, 
course, and prognosis of the disease. 

This is to be expected when we consider that the disease produced 
by the tubercle bacilli depends on the interaction of two forces of 
inconstant intensity, viz.: 

1. On the Intensity of the Infection.—This depends on the number 
of bacilli which have entered the body; their virulence which we 
know is variable, depending on the type and the condition under 
which they existed before entering the body, etc., and on the portals 
of entry. It is doubtful whether infection by inhalation will produce 
the same clinical picture as infection by ingestion or by inoculation; 
whether hematogenous tuberculosis will produce the same symptoms 
as aérogenous or lymphogenous infection. 

2. On the resistance of the host, which is also an inconstant value, 
depending as it does on so many variable, complex, certain and uncer- 
tain, constant and transient conditions which cannot always be defined 
clearly. Thus, the effects of the infection depend on the dose, and 
also on the age at which it has taken place. During the first six or 
twelve months of life massive infection produces a different disease 
from that of the succeeding years of childhood. Acute miliary tuber- 
culosis is common at the former age, while tuberculosis of the glands, 
bones, and joints is mostly seen at the later ages. Primary infection 


368 THE CLINICAL FORMS OF PHTHISIS 


of an adult is usually followed by clinical phenomena which differ 
markedly from those seen in individuals who were presumably infected 
during childhood, and the bacilli remained dormant for many years. 
We have already discussed the effects of preéxisting diseases on the 
type and course of phthisis. 

“To speak of pulmonary tuberculosis as an entity,” says von Hanse- 
mann, “‘and to describe it as one disease, caused by the tubercle 
bacillus is hardly conceivable. One has to compare pure miliary tuber- 
culosis of the lungs with chronic indurative phthisis, and the latter 
with acute florid phthisis, or caseous hepatization of the lungs, to find 
clearly that they are different pathological pictures which defy all 
comparisons. For these reasons it is altogether impossible to speak 
simply of pulmonary tuberculosis and thereby retain a clear survey 
of the different forms of the disease. In reality we are compelled to 
draw a sharp line of demarcation between these different forms of 
the disease, even when we are inclined to consider the tubercle bacilli 
as the underlying etiological cause of all the forms of the disease.” 

The Stages of Phthisis.—EKarly writers on phthisis, who were 
innocent of modern methods of diagnosis, felt constrained to differ- 
entiate various forms of the disease as they saw it clinically. They 
divided it into three stages: Phthisis incipiens, phthisis confirmata, 
and phthisis desperata. Bayle, in the first decennium of the nineteenth 
century, added a fourth stage, Phthisis occulta, or germe de la phtisie, 
which corresponds to the modern pretuberculous stage, when the 
tubercles in the lung are too few to produce symptoms. Laennec, 
who was an excellent and pioneer pathologist and clinician, having 
invented auscultation, divided phthisis into three stages, basing his 
classification on anatomical grounds. He divided phthisis into: 
First stage, the accumulation of the tubercles, which betray themselves 
by bronchophony and dulness over the affected area; second stage, 
softening of the lesion, producing bronchial breathing, coarse rales 
and pectoriloquy; and third stage, the elimination of the softened 
area, leaving pulmonary excavations which may be found by careful 
physical exploration. 

This division of phthisis into three or four stages has remained 
to date not only among the laity, who fear the second and third 
stages, but also among physicians, who are always aiming at discover- 
ing the disease in the pretuberculous stage, or at least in the first, 
or incipient stage. Some even maintain that the disease is curable 
only at this stage. That this is not always true will be shown later on. 


OFFICIAL CLASSIFICATION OF THE STAGES OF PHTHISIS. 


With the advance of knowledge of the clinical manifestations and 
the methods of recognition of the disease, the stages into which phthisis 
is divided remained practically the same. They have only been more 


1 Berl. klin. Wehnschr., 1911, 47, 1. 


OFFICIAL CLASSIFICATION OF STAGES OF PHTHISIS 369 


exactly defined. In Germany the classifications of Turban and 
Gerhardt have gained wide acceptance, while in this country the 
American Sanatorium Association, and the National Tuberculosis 
Association have adopted the following classification, which of late 
has also been in vogue in most Anglo-Saxon countries: 

Incipient.—Slight initial lesion in the form of infiltration limited 
to the apex of one or both lungs or a small part of one lobe. No 
tuberculous complications. Slight or no constitutional symptoms 
(particularly including gastric or intestinal disturbance or rapid loss 
of weight). 

Expectoration usually small in amount or absent. 

Tubercle bacilli may be present or absent. 

Moderately Advanced.— No marked impairment of function, either 
local or constitutional. Localized consolidation moderate in extent 
with little or no evidence of destruction of tissue or disseminated 
fibroid deposits. No serious complications. 

Far Advanced.— Marked impairment of function, local and con- 
stitutional. Localized consolidation intense, or disseminated areas of 
softening, or serious complications. 

Shortcomings of the Official Classifications.—If the object of this 
classification is to define the prognosis of phthisis, it fails utterly. A 
patient with a “slight initial lesion in the form of an infiltration of the 
apex” has not always a greater expectation of life than one having 
“marked local impairment of function and extensive destruction of 
tissue.” In fact, in acute miliary tuberculosis of the lungs the lesion 
is so slight that it often cannot be localized during life. On the other 
hand, many cases of phthisis with extensive excavations have a better 
outlook, at least as regards duration of life, and even as regards regain- 
ing efficiency, than some with limited lesions at one apex, without 
expectoration of tubercle bacilli, but with evidences of severe toxic 
activity. Moreover, it is clinically wrong to put into one class the 
incipient cases showing no fever, no tachycardia “at any time during 
the twenty-four hours,”’ no gastric or intestinal disturbances, no rapid 
loss of weight, ete., which are evidently cases of abortive tuberculosis, 
if at all actively tuberculous, with those having lesions limited to one or 
both sides, and who do show constitutional symptoms of toxemia. 
The former will recover within a few months under any rational form 
of treatment, or spontaneously, while the latter may not, even with the 
most rigid institutional, climatic, dietetic, or specific treatment. 

Physicians having opportunities to observe many tuberculous cases 
are struck with the fact that the prognosis, immediate and ultimate, 
does not entirely depend on the changes in the breath sounds, the 
presence or absence of rales, and signs of excavations in the lungs. 
The constitutional symptoms, such as fever, pulse-rate, presence or 
absence of dyspnea, gastric disturbances, and, above all, the resistance 
of the patient, play a greater role in the ultimate outcome of a case 
than the anatomical changes. 

24 


370 THE CLINICAL FORMS OF PHTHISIS 


In order that a case may be considered “incipient,” according to 
this classification, and nearly all others which have been devised, the 
constitutional disturbances must be slight or absent. ‘Thus, in the 
definition of terms it is stated that “the impairment of health may be 
so slight that the patient does not look or feel sick in the ordinary 
sense of the word.” The pulse should not exceed 90 per minute and 
the temperature 99.5° F., and the sputum may be negative. The 
physical signs consist in “slight prominence of the clavicle, lessened 
movement of the chest, narrowing of the apical resonance with les- 
sened movement of the base of the lung, slight or no change in reso- 
nance, distinct or loud and harsh breathing with or without some 
changes in the rhythm (7. e., prolonged expiration), vocal resonance 
possibly slightly increased; or fine or moderately coarse rales present 
or absent. If sputum contains tubercle bacilli, any one of these.” 
Considering that the apex is defined as “that portion of the lung 
situated above the clavicle and the third vertebral spine,” it is clear 
that the lesion must be quite limited, often of the type considered 
“dubious” by many competent clinicians. 

All these symptoms, or absence of constitutional symptoms and 
signs in the chest, may be found in a large proportion of persons in all 
walks of life, working hard at their occupations, who, if followed for 
many years, are not found to develop active phthisis. People with 
collapse induration often show more distinct physical signs at one 
apex, yet they are not phthisical. In the instructions given to exami- 
ners of recruits, such individuals were ordered taken into the armies 
in every European country, as well as the United States. 

On the other hand, a really phthisical person showing so few signs 
on physical exploration, but in whom the disease is pursuing an acute 
or subacute course, may be carried off much quicker than many with 
extensive involvement, but manifesting a tendency to chronicity of 
the process. 

It cannot be denied that these three or four stages of tuberculosis 
are altogether arbitrary. We cannot often separate them by sharp 
lines of demarcation and say “this is a first stage case,” or “this case 
is passing from the second into the third stage,’ etc. There are 
always transitional forms. There are also numerous cases showing 
healed lesions which at the time of activity were in the third stage, 
but give no more trouble—while an initial lesion in the other lung is 
responsible for the disease for which the patient consults the physician. 
Such cases, incipient in the true sense of the word, must be considered 
far advanced according to this classification. It is also a fact that, for 
phthisis to end fatally, it is not necessary that the lesion in the lung 
should soften and produce a cavity; caseation alone, when extending 
rapidly, may kill; the patient has thus not reached the third stage, 
yet he dies. On the other hand, we have numerous patients who, 
despite the fact that they have more or less extensive excavations in 
the lungs, are in fact in the third stage of phthisis, yet they feel well, 


OFFICIAL CLASSIFICATION OF THE STAGES OF PHTHISIS 371 


and are even efficient at their occupations, and when they finally die 
the cause may be another disease. 

For these reasons some clinicians have been constrained to distinguish 
the various forms of phthisis met with in practice into different clini- 
cal entities. Thus, even the classification mentioned above considers 
acute miliary tuberculosis as a distinct disease. Other authors, like 
Alfred Loomis, Williams, Andrew Clark, Douglas Powell, etc., have 
described fibroid phthisis—which in the above classification would 
always be included among the advanced cases—as a distinct disease. 

Many writers on this subject have gone much further and distin- 
guished not only acute and chronic forms of the disease but have also 
described congenital, or hereditary and acquired forms of the dis- 
ease; phthisis in arthritic, gouty, diabetic, nephritic, alcoholic, or 
syphilitic subjects; also according to some prominent symptoms, such 
as hemorrhagic, bronchitic, bronchiectatic, pleuritic phthisis. In 
accordance with certain etiological factors, there has been described 
phthisis in workers at dusty occupations, such as miners’ phthisis, etc. 
Finally tuberculosis of the lungs in children has always been consid- 
ered as presenting a different clinical picture from that in the adult; 
while in aged persons the symptomatology of phthisis differs from 
that in younger individuals. 

Classification in the Present Work.—The classification of the 
diversity of clinical types of tuberculosis of the lungs, to be of practical 
value, if itis to be attempted at all, must havea prognostic value. For 
this reason the acute forms of the disease are to be separated into a class 
by themselves, as has, in fact, been done by all writers on the subject. 
In chronic phthisis the ultimate outcome of the disease depends 
mainly on the relative intensity of the two processes in the lungs, the 
destructive and the reparative, the former manifesting itself by 
caseation and softening, and the latter by the formation of fibrous 
tissue which limits the destructive process and even heals the lesion 
by cicatrization. Both processes, fibrosis and necrosis, are caused by 
the tubercle bacilli. And inasmuch as there are many cases in which 
fibrosis dominates the anatomical changes in the lungs, and the 
symptoms thus produced differ from those in which the caseating 
process predominates, it is clear that there is justification for separation 
of fibroid phthisis into a distinct class of the disease. This justification 
is fortified by the fact that the prognosis of fibroid phthisis is distinctly 
more favorable than that of chronic caseous phthisis, and the treatment 
indicated is different from that in other forms. 

In common chronic phthisis we find that among the cases which 
have been described as “incipient” there are many which show a 
marked tendency to cicatrization of the lesion, spontaneously, or after 
some treatment for a few months. In the vast majority of cases 
this form of phthisis is not at all recognized and only at the autopsy 
some scars or calcified foci are found in the lung or pleura showing 
that the person had survived a tuberculous lesion. To treat these 


3/2 THE CLINICAL FORMS OF PHTHISIS 


cases in the same manner as we treat common chronic phthisis is 
wrong. We should, when diagnosticating a case of this kind, tell the 
patient that his malady is relatively trifling, and that he will recover 
within a few months, if he observes ordinary hygienic and dietetic 
rules. We can often also: spare him the trouble and the economic 
danger of giving up his business which is usually necessary in cases 
of chronic phthisis. We have therefore described abortive tubercu- 
losis as a distinct clinical type of the disease. 

Most of the victims of tuberculosis who succumb to the disease, or 
who suffer from it for long periods of time, even if they recover, are 
affected with chronic phthisis. This disease is characterized by an 
undulating course, marked by periods of quiescence of longer or 
shorter duration, and interrupted by periods of acute, or subacute 
exacerbations. In fact, it may be stated that acute progressive 
phthisis, or galloping consumption, consists clinically in an acute 
exacerbation of the disease which is not followed by a period of quies- 
cence. In the chronic type of the disease, proper and timely treatment 
may save the patient, while negligence in this regard is apt to prove 
disastrous. [or this reason it is imperative that it should be recognized 
as early as possible. We have therefore divided the subject into two 
parts: incipient phthisis and advanced phthisis. The former, if 
recognized in time, and appropriate treatment applied, may often be 
aborted; or acute exacerbations leading to irreparable damage of the 
lungs and other organs and functions may be prevented. The latter, 
when properly cared for, may be kept in check so that acute exacerba- 
tions occur less frequently, or not at all, and cicatrization of the lesion 
goes on unhindered. 

We also know that tuberculosis in children is anatomically, and also 
clinically, not of the same character as that in adults. In the former 
the glands, bones and joints, while in the latter the lungs, are mainly 
the organs which bear the brunt of the infection. Indeed, consider- 
able harm is done to children by treating them for chronic pulmonary 
tuberculosis which, before the eighth year of life, they practically 
never have. For this reason, the disease as it occurs in infants and 
children merits separate description. Because in infancy the infec- 
tion is usually followed by acute manifestations, while in children 
between two and ten years of age chronic disease of the glands occurs, 
we shall speak of tuberculosis in infants and tuberculosis in children. 

Finally, it is now known that phthisis occurs in the aged just as 
frequently as in younger individuals, but that it is not recognized 
very often because of the peculiar symptomatology it presents. Aged 
consumptives, believing that they only suffer from chronic bronchitis, 
asthma, or pulmonary emphysema, are sources of infection to an 
extent not so fully appreciated as they deserve. We have there- 
fore devoted a special chapter dealing with tuberculosis in the aged, 
pointing out its clinical manifestations. 

While in nearly every case of pulmonary tuberculosis the pleura is 


OFFICIAL CLASSIFICATION OF THE STAGES OF PHTHISIS 373 


implicated in the process, more or less, there are cases in which the 
disease begins in the pleura and shows no tendency to spread into the 
pulmonary parenchyma. In others, the pleural lesion is the main one 
with which the patient has to cope. Moreover, it appears that the 
vast majority of pleurisies which had formerly been considered “idio- 
pathic,” are in reality tuberculous in character. For these reasons a 
book on pulmonary tuberculosis is incomplete unless a detailed account 
is given of tuberculosis of the pleura. 

These forms of phthisis do not exhaust the subject of the clinical 
polymorphism of this disease. There are many other types which 
may be appreciated when carefully studying the cases, while quite 
often these types overlap one another to an extent as to render it 
difficult to decide to which class a case belongs. But for practical 
purposes these clinical types are sufficient. They assist in appreci- 
ating the course of the disease when it occurs, and give us hints for 
prognosis and treatment which are invaluable, and which cannot be 
had when pulmonary tuberculosis is considered as a single clinical 
entity. 

We shall therefore describe phthisis under the following headings: 

1. Chronie phthisis, incipient stage. 

2. Chronic phthisis, advanced stage. 
Abortive pulmonary tuberculosis. 
Fibroid phthisis. 

Acute forms of phthisis. 
Pulmonary tuberculosis in children. 
Phthisis in the aged. 

Tuberculosis of the pleura. 


WIM Ie w 


CHAPTER XIX. 
CHRONIC PHTHISIS, INCIPIENT STAGE. 


INCIPIENT PHTHISIS. 


Onset.—A lay writer,' describing his own, subsequently fatal, case 
of phthisis, in speaking of his “initiation into T. B.,” says: “The 
entrances are innumerable, however sole the exit. Indeed, the initia- 
tion varies so widely that one would not be far wrong in saying that 
it is never twice the same. Yet many initiations have certain features 
in common, and in a general way it may be said that all belong to 
one of two great classes—the sudden and the protracted.’ No 
physician, however extensive his experience with phthisis, could do 
more justice to the subject, or make a better generalization of the 
various ways in which phthisis is likely to begin. 

A sudden or abrupt onset of phthisis is infrequent, but it does occur. 
We meet with patients who have been in the best of health; have no 
ascertainable hereditary taint; have not come into immediate or 
intimate contact with a consumptive, so far as they can remember; 
have not overworked, not suffered from exposure, but they suddenly 
begin to cough, lose weight, have fever, feel tired at the least exertion, 
and a careful physical examination reveals a small, but progressive 
lesion at one apex. We meet with others who, without any premoni- 
tory symptoms, without any exciting cause, suddenly perceive a warm 
sensation in the throat, cough, and bring up a mouthful of blood. The 
hemoptysis may be scanty or copious, but the signs elicited while 
examining the chest leave no doubt that it is derived from a pulmonary 
lesion, and the subsequent course of the disease proves conclusively 
that we are dealing with phthisis. Still others, after an indiscreet 
exposure to the vicissitudes of the weather, or after a cold bath to 
which they are not accustomed, begin to cough and are treated for a 
“cold,” “grippe,” ete., for some time. But the symptoms fail to 
ameliorate in spite of careful treatment, when one day a careful 
examination of the chest shows a distinct lesion, or a bacteriological 
examination of the sputum reveals the presence of tubercle bacilli. 
In some, exposure may bring on an attack of pleurisy, dry or with 
effusion, the subsequent course of which is distinctly that of phthisis. 

But in a large proportion of cases the disease develops slowly, insidi- 
ously—the initiation is protracted, as our lay friend said. For months, 
perhaps a year or two, the patient has not been well. Hehas been“ sub- 





1 Atlantic Monthly, June, 1914, 113, 747. 


INCIPIENT PHTHISIS 375 


ject to colds,” and in autumn or winter he passed through one or more 
attacks of “ grippe,’’ bronchitis, ete., with cough, expectoration, fever, 
malaise, etc., but he soon recuperated and worked more or less effi- 
ciently at his vocation. Finally one attack sticks and he does not 
improve, notwithstanding the remedies which were formerly effective. 

In young men the symptoms which we are apt to label as “neuras- 
thenia,” may have been present for a year, two, or more. What was 
most annoying, and could not be relieved by the usual treatment 
instituted, was the languor, the tired feeling which overwhelmed the 
patient before his day’s work was at an end. He may be complain- 
ing of cardiac palpitation, indefinite pains in the chest, some cough 
in the morning, ete. But on the whole he considered himself “run 
down,” and sadly in need of a rest. 

In young women the subjective and objective symptoms of chlorosis 
may have been present for months or years. An examination of the 
blood has, indeed, shown a low percentage of hemoglobin, and large 
doses of some iron preparation have been used. Some have had 
irregularities in the menstrual function, perhaps amenorrhea for 
several months, and even this was attributed to the anemia. But 
then they begin to cough; and the cough persists in spite of treat- 
ment, when an examination of the chest, or of the sputum, tells the 
story. 

Others have been “run down” from overwork, physical or mental, 
for a long time till it is discovered that the cause of their debility is 
located in the lungs. In many patients the symptoms of dyspepsia 
are so pronounced as to preclude a careful examination of the chest 
and they are treated for a long time for “stomach trouble.” 

This does not exhaust the variety of symptoms which may slowly, 
but surely, usher in phthisis. But numerous as they are, they have 
certain features in common which characterize phthisis in the vast 
majority of cases, so that if this disease is only borne in mind—and it 
should, considering its great prevalence—more really incipient cases 
would be recognized than at present. These clinical phenomena will 
now be discussed. 

Symptoms.—Practically all patients with incipient phthisis cough 
at a very early stage of the disease, and the cases without cough, 
which have been mentioned by various authors, are rare clinical 
phenomena, at least they are exceedingly rare among persons under 
fifty years of age, and may be disregarded. It was already stated that 
patients who claim that they do not cough are usually individuals 
who overlook a mild cough, but those around them are apt to notice 
that they do, and in doubtful cases it is advisable to inquire among 
those who live with the patient. 

A person who never coughed, but after a “cold”? coughs for more 
than two weeks, should excite interest and careful study. If he 
vomits after fits of coughing, tuberculosis is to be strongly suspected. 
Paroxysmal coughing spells are also apt to take place during the night 


376 CHRONIC PHTHISIS, INCIPIENT STAGE 


and keep the patient awake. Very little expectoration is apt to be 
brought up at this period—at most some viscid mucus which contains 
no or few tubercle bacilli, nor elastic tissue, though animal inoculation 
may be effective in disclosing the tuberculous nature of the trouble. 

Languor is a constant symptom at a very early stage—the patient 
feels tired in the morning at rising, but recuperates after working for 
afew hours. But in the later part of the afternoon he feels fatigued, 
often drowsy, inclined to sleep. It is this tired feeling which is to be 
held responsible for the fact that so many patients are erroneously 
treated for neurasthenia and psychasthenia, or for a “nervous break- 
down,” for a long time until the true nature of the disease is finally 
ascertained. 

Anorexia is an inconstant and variable symptom of incipient phthisis. 
In some, especially in youthful subjects, it is very frequent and, 
coupled with anemia, constipation, ete., is the cause why so many 
are treated for chlorosis, gastritis, etc. There are many cases in 
which the appetite is well retained and, when not “dieted” with a 
view of improving nutrition and digestion, but urged to eat well and 
plenty of the foods they are accustomed to eat, they do not lose in 
weight, but may gain, even when the process in the lung goes on 
actively. 

But in the majority of cases a persistent loss of weight is noted at 
this period. In some it is slow, only one pound per week on the aver- 
age, while in others it is more rapid and during the first two months 
fifteen to twenty pounds may be lost. 

The activity of the process is best estimated by the fever, which is 
never absent. It may be slight, only 1° elevation in the afternoon, but 
it can be found in every case by the judicious use of the thermometer. 
A subnormal temperature during the early morning hours, best looked 
for by taking it per rectum before the patient leaves his bed, is very 
frequently observed, and of immense diagnostic significance. In many 
the fever subsides when the patient is kept in bed for a couple of days 
but reappears as soon as some exercise is allowed. In those with 
an apparently normal temperature, fever may be provoked by walking 
or any other form of exercise, as was already discussed in detail (see 
page 218). In women, the fever may appear only during the menstrual 
period, or a few days before. 

In a large number of cases pyrexia is considerable even at this 
early stage, up to 102° or 103° F. in the afternoon and evening and, 
measured by comparison with the subnormal temperature in the 
early morning hours, it is quite high. The “reversed type’ of fever, 
with a rise in the morning, is occasionally seen. 

A significant diagnostic point is that with high fever the patient 
may not be prostrated as is the case with adults who have fever due to 
other causes. Moreover, the patient may have a fair, even a good 
appetite, despite the fact that the thermometer registers 102° or 103° 
F., which is very rare in fevers due to other causes. During the 


INCIPIENT PHTHISIS BIes 


afternoon access of the fever, the patient, otherwise pale, becomes 
flushed, often only one cheek is red, he is tired, and disinclined to 
work. But he may keep on working, as was already stated. 

Nightsweats make their appearance in a large proportion of cases 
at this stage. In some they are slight, while in others I have met 
with profuse nightsweats during the first two weeks of active symp- 
toms. They perspire also at the least exertion or excitement, and 
during a medical examination it is not rare to see large drops of sweat 
dribbling down the sides of the chest from the axille. 

A constant accompaniment of fever in incipient cases is tachycardia. 
A ease of active phthisis with a pulse-rate below 80 per minute is exceed- 
ingly rare. In some the heart action is so rapid that they are treated 
for heart disease, or for hyperthyroidism in case the thyroid is enlarged, 
which is not rare, especially in youthful individuals. While in the 
early morning after a refreshing sleep the pulse-rate may be normal, 
the least exertion or excitement will raise it up to 90, 100 or more. 
Instability of the pulse is characteristic of phthisis. In youthful sub- 
jects the tachycardia is apt to be more pronounced than in persons 
over twenty-five years of age. The blood-pressure is low and a regis- 
tration less than 80 mm. of mercury is quite common. 

Symptoms referable to the respiratory system may not be seen at 
this stage, excepting the cough and, at times, the intermittent hoarseness, 
which is usually due to a laryngeal catarrh, or pressure on the laryngeal 
nerve, and hardly ever to infiltration of the larynx. At times we see 
patients who suffer from more or less pronounced pains in the chest, 
especially under the scapula, or in the shoulder. 

Hemoptysis is quite frequent at this stage. As was already stated, 
statistics taken of large numbers of patients show that about 10 per 
cent. of cases begin with hemorrhage. They are the lucky ones, 
because this clears up the case, and proper measures are promptly 
taken. But many of these initial hemorrhages were actually preceded 
by a train of symptoms, such as fever, tachycardia, ete., to which the 
patient paid no attention. However, in about 25 per cent of cases 
more or less blood-spitting occurs at the time the disease is recog- 
nized. It may be only blood-tinged sputum, a mouthful or two of 
blood, or even a profuse hemorrhage. It will bear repetition that 
these initial hemorrhages are practically never fatal. 

Physical Signs.— With any or all of these symptoms a diagnosis of 
incipient tuberculosis should not be made unless physical exploration 
of the chest discloses a localized lesion in the lungs. 

Inspection.—Inspection yields excellent diagnostic criteria in most 
cases at this early stage. Inasmuch as most of the incipient cases 
are really recrudescences of old quiescent lesions in many instances 
dating back to childhood, we find in many atrophy of the muscles over 
the site of the lesion. ‘The sternocleidomastoid, the scaleni and trape- 
zius, etc., may be smaller than those on the opposite side, and softer, 
or even flabby to the touch. This is more important to look for than 


378 CHRONIC PHTHISIS, INCIPIENT STAGE 


the form of the chest, which may be normal, flat, rachitic, ete., without 
influencing the diagnosis. With the atrophy of the muscles there is 
usually seen a slight shoulder-droop and an excavation of the supra- 
clavicular or supraspinous fossa, or at least some flattening and defec- 
tive motion or lagging of the part of the chest harboring the lesion. 
This asymmetry, flattening and lagging, is very easy to detect if care- 
fully looked for and is, when found, of immense diagnostic importance, 
provided occupational influences are excluded. 

In more recent lesions, or whenan old and perhapsa healed lesion exists 
in one side, but the outbreak of phthisis is due to a new lesion in the 
opposite side, which is very frequent, we find the muscles over the site 
of the active new infiltration are tense and rigid, standing out promi- 
nently. But this is after all not very frequent, which goes to show that 
most of the incipient cases are really due to reawakening of old, 
smouldering, tuberculous processes in the lung. 

Percussion. — As was already stated, there are very few cases of active 
incipient tuberculosis in which no signs of an infiltration can be dis- 
covered by careful and gentle percussion. We almost invariably find 
some airless pulmonary tissue, or shrinkage of one apex manifesting 
itself by a short note, or by pulmonary retraction. The height of the 
apex may be less than that of its mate on the opposite side, or its width 
may be less, as determined by Kr6énig’s method of percussion. We 
may also find, though not so often as Kroénig believed, that the base 
on the affected side is somewhat retracted. Immediate percussion of 
the clavicle, as was first practised by Laennec, may at times easily 
reveal a lesion beneath that bone. 

In my own experience, percussion signs are more often found over 
the posterior aspects of the apices than anteriorly. While over the 
supraclavicular region we may find that the width of the resonant 
area is less than that of the other side, it is easier and less time-con- 
suming to map out the mesial lines of demarcation between resonance 
and dulness in the supraspinous fossee, and over the site of the lesion 
this line is usually dislocated outward. 

It is also easily ascertained whether the height of the apices poste- 
riorly shows any asymmetry. Ata very early stage we find that while 
over the unaffected apex the resonance reaches as far as the interval 
between the seventh cervical and first thoracic spines, that of the 
affected apex is much lower. I have found these changes at times 
before any auscultatory signs made their appearance. 

The changes in pitch, duration and intensity of the note obtained at 
this stage are of less significance than those of shrinkage just spoken of, 
and they depend too much on the personal equation of the observer 
to have important clinical bearings. Thus, we often find that a con- 
tracted apex is altogether hyperresonant, or even tympanitic on per- 
cussion, and by comparison the unaffected side appears to emit a defec- 
tive note. The stories told in text-books about two equally competent 
clinicians localizing an apical lesion by percussion, and each finding 


INCIPIENT PHTHISIS 379 


it in another side, are undoubtedly based on these facts. It is generally 
due to faulty interpretation of tympany caused by relaxation and 
hyperfunction of the lung tissue around conglomerations of tubercles, 
as has already been shown. The discordance may also be due to an 
old and cicatrized lesion on one side, while the new and active lesion 
is in the opposite side of the chest. 

Of greater importance is respiratory percussion. The patient is 
asked to inspire or expire and hold his breath, and we percuss during 
each phase of respiration. In health the note is clearer during full 
and held inspiration, while over an infiltrated apex a long and held 
inspiration gives a duller note than found over the opposite, unaffected 
side. 

Of the various seats of election of dulness in incipient phthisis which 
have been described by Lees,! Riviere,” and others, the sites I have been 
able to find impaired in most cases at a very early stage are the supra- 
spinous fossve, near the spine, and beneath and above the inner third 
of the clavicle. Persistent, impaired resonance in any of these places, 
when accompanied by constitutional symptoms of phthisis, is of diag- 
nostic significance. Impaired resonance elicited with hooked-finger 
percussion between the heads of the sternocleidomastoid immediately 
above the clavicle on one side is very often found. 

Auscultation.—It is not generally appreciated that the earliest 
changes in the respiratory sounds in phthisis are modifications of 
the inspiratory murmur, while changes in the expiratory murmur 
usually indicate a more or less advanced stage of the disease. At a 
very early period of the disease the inspiratory murmur loses its soft, 
breezy character and becomes rough or granular, an indication of par- 
tial stenosis of the bronchioles supplying the affected part of the lung, 
or unequal respiratory movement of the infiltrated lung area. In 
many cases the inspiratory murmur is feeble, at times even absent, 
over a limited area corresponding to the area of impaired resonance, 
while the whispered voice is transmitted clearly. But the most com- 
mon sign of an early lesion is interrupted, or cog-wheel, breathing; the 
inspiratory sound is broken up into several parts so that it appears 
jerky. Either of these types of altered inspiratory murmur may be 
audible long before the expiratory murmur is In any way changed. 

The most common seats of the changed breath sounds are poste- 
riorly near and above the spine of the scapula, the “alarm zone’”’ of 
Chauvet,’ and rarely in front immediately beneath the inner third of 
the clavicle. It is located posteriorly as follows: From the space 
separating the spinous process of the seventh cervical from that of 
the first thoracic vertebree, a line is drawn as far as the tubercle of 
the trapezius on the spine of the scapula. From the middle of this 
line, taken as a center, a circle is described with a diameter equal to 


1 British Med. Jour., 1912, 2, 1268. 
2 Harly Diagnosis of Tubercle, London, 1914, p. 25. 
3 Le monde médical, 1913, 22, 1121; La Clinique, 1913, 8, 437. 


380 CHRONIC PHTHISIS, INCIPIENT STAGE 


that of a silver dollar. The circumference of this circle forms the 
boundary of the “zone of alarm” (Fig. 83). When heard at any of 
these points during ordinary breathing, and repeatedly found on 
several examinations, not decreasing in intensity but on the contrary 
becoming more and more pronounced, rough and cog-wheel breathing 
are good signs of incipient infiltration of an apex, provided of course, 
that the constitutional symptoms show activity; otherwise they may 
be indications of old and cicatrized lesions. We have already stated 
that at times feeble breath sounds are found; they may be of a blow- 
ing or even of a bronchial character, and some crackling may be 
audible at the end of inspiration. 





Fig. 83.—1, The “alarm zone’’; 2, the space between the spinous processes of the 
seventh cervical and first dorsal vertebrze; 3, the tubercle of the trapezius. 


Rales are not heard at all over really incipient lesions. Occasionally 
some sibilation is audible, but this is usually transitory and disappears 
after the patient takes a deep breath. At most, some dry crackling 
may be brought out when the patient coughs vigorously. When crepi- 
tant, and especially moist subcrepitant, rales are audible, we are dealing 
with an extensive lesion of some duration. 

In some cases we hear at a very early stage during expiration a 
hemic murmur originating in the subclavian artery and ascribed to 
kinking of that vessel by the tuberculous infiltration, or by shrinking 


INCIPIENT PHTHISIS 381 


lung. But it is by no means pathognomonic of phthisis because it is 
heard in many apparently healthy persons. 

The whispered voice is very often transmitted more or less clearly 
over consolidated areas fo lung tissue, and when heard when the chest- 
piece of the stethoscope is pressed firmly over the skin of the chest, it 
is of the same diagnostic significance as impaired resonance, with 
which it usually runs parallel, as bas been pointed out by Sewall.! 
But it must be emphasized that its absence does not exclude a tuber- 
culous lesion. The voice sounds are transmitted only when the con- 
solidated tissue is located superficially or subpleurally. When it is 
centrally located, screened by air-filled lung tissue, the voice sounds 
may be normal. 

To be of diagnostic significance in early phthisis, the auscultatory 
signs must be localized over one apex, circumscribed, fixed and per- 
sistent for some time, and not influenced by cough and strong respira- 
tory efforts, excepting clicks and rales which may be brought out by cough. 
Evanescent changes in resonance and breath sounds may be found 
in many apparently healthy persons. It is for this reason that those 
who attempt to make a final diagnosis of incipient phthisis during one 
examination meet with so many failures. 

Elements of Diagnosis of Incipient Phthisis.—Just as the general 
and constitutional symptoms, such as cough, fever, tachycardia, ema- 
ciation, etc., are insufficient to decide a case till the lesion is localized 
in the lung, so are the signs obtained by physical exploration of the 
chest inadequate, even when marked, to prove that we are dealing with 
a case of active incipient phthisis. Only the combination of both 
groups of clinical data gives solid support for diagnostic inferences. A 
skilled diagnostician may easily diagnosticate a case of advanced 
phthisis by looking at the pathognomonic facies of the patient, from the 
history and course of the disease, or from auscultatory findings alone, 
and only rarely err. But in incipient phthisis it is the correlation of 
all available clinical data, the history, the symptomatology and course 
of the disease, combined with the findings of physical exploration of the 
chest and bacteriological as well as roentgenological data that can be 
expected to clinch the diagnosis. 

The signs enumerated above—defective resonance, narrowing of the 
resonant areas over one apex, feeble, rough, granular or cog-wheel 
breathing, or even rales, may each be found in persons of excellent 
health, at least such as are not actively tuberculous. This is because 
old and healed lesions, tuberculous and others, leave traces behind 
them which alter permanently the air content of the pulmonary par- 
enchyma and diagnostic methods in vogue disclose these conditions. 

Sources of Errors.—I am not prepared to state that the proportion 
of diagnostic errors made while attempting to recognize phthisis in its 
very incipiency is greater than in other diseases; in fact, I am convinced 





1 Jour. Am. Med. Assn., 19138, 60, 2027, 


382 CHRONIC PHTHISIS, INCIPIENT STAGE 


that it is not. But in phthisis, owing to its great prevalence and its 
social and economic aspects, as well as its insidious onset, the oppor- 
tunities for making mistakes are immense. It is for this reason that 
the sources of error must be emphasized. 

Bias is more often a source of error in phthisis than in any other 
disease. Especially is this the case when there is a history of exposure 
to infection. To my mind this is one of the greatest fallacies we have 
to cope with. It must always be remembered that in large industrial 
cities everyone is exposed to infection and is, in fact, infected with 
tubercle bacilli before he passes his fifteenth vear. On the other 
hand, marital phthisis is less frequent than would be expected if every 
adult exposed to tuberculosis would invariably or in most cases become 
phthisical. Excepting in young children a case must therefore be 
judged on its clinical manifestations and not on the fact that the 
patient came into contact with a consumptive. 

Tubercle Bacilli.— The diagnosis of phthisis rs clinched by the finding 
of tubercle bacilli in the sputum, but the disease vs not at all excluded by 
negative bacteriological findings. Unfortunately, too many wait rather 
long for the bacilli, thus losing valuable time which often cannot 
be reclaimed by any known means. Phthisis begins as an infiltra- 
tion, and only when softening has taken place and the products of 
tissue disintegration are eliminated through a bronchus can tubercle 
bacilli be found in the sputum. Under the circumstances, wazting 
for tubercle bacilli to make their appearance in the sputum is just as 
hazardous as waiting for pus to make its appearance through a fistula 
or sinus before making a diagnosis of a tuberculous joint. 

In very rare instances there are errors of quite a different nature. 
Tubercle bacilli may be found in the sputum of persons who are not 
actively tuberculous. Of course, from the practical standpoint tubercle 
bacilli in sputum are an indication that they are in all probability 
derived from a tuberculous lesion in the lower respiratory tract. But 
in New York City we meet with numerous persons who have reports 
from some private, as well as from the municipal laboratory, stating 
that the sputum of the bearer had been examined and found to con- 
tain tubercle bacilli. Yet, without any treatment or special care, they 
have kept at work for years and felt well. Indeed, many cases are 
admitted to sanatoriums solely on the strength of positive sputum 
findings, to be declared non-tuberculous after careful observation. 

The reasons for this anomaly are to be sought for in several facts 
which have not been emphasized as strongly as they deserve. I have 
no doubt that in busy laboratories mistakes are liable to happen in 
handling the sputum bottles, in numbering the slides, or while enter- 
ing the findings in the reports. In banks, where the clerks are just as 
careful as laboratory workers, mistakes occur at times. Even con- 
ceding that the number of such mistakes is comparatively negligible, 
in the individual case it may count very much. 

We have already spoken of the acid-fast rods which simulate tubercle 


INCIPIENT PHTHISIS 380 


bacilli and which are found in butter and milk, on graminacea, in the 
soil, in dung and manure, and even in tap water supplied through metal 
pipes. These bacilli are dead, or non-pathogenic to guinea-pigs, but 
they give the usual staining reactions. Then we may have the smegma 
bacilli which have been mistaken for tubercle bacilli and thus have 
led to erroneous diagnosis and extirpation of healthy kidneys. There 
are also the acid-fast lepra bacilli, the microdrganisms which greatly 
resemble them and are found in the secretion of the mucous membrane 
of the nose, also the acid-fast rods found in the saliva and the secretions 
in cases of bronchitis and pulmonary gangrene. L. Napoleon Boston! 
found acid-fast bacilli in patients suffering from acute colds and 
influenza, and disappearing during convalescence. But most of these 
microérganisms are difficult to differentiate from tubercle bacilli 
microscopically, through culture and animal inoculation. 

It has recently been found that the spores of lycopodium are acid- 
fast, so that persons taking pills covered by that substance may impart 
some of it to the sputum and thus lead to error. 

There is a possibility that the acid-fast rods or specks found in the 
sputum may not have been there before it left the bronchial tubes and 
trachea, but got into the sputum while it was passing through the 
pharynx, mouth or lips, especially in persons living in houses inhabited 
by careless consumptives. I have repeatedly observed this to be a 
fact in consorts of tuberculous patients. Tubercle bacilli are found in 
the sputum—usually saliva—but they keep up in good health. It is 
also important to mention that ordinary smear preparations are less 
likely to lead to errors of this sort than the antiformin method. 

To be sure, the most reliable sign of phthisis is tubercle bacilli in 
the sputum, and I do not at all intend to underestimate its far-reach- 
ing significance. Statistically, the chances of error are undoubtedly 
insignificant, and a laboratory may be proud that among several 
thousands of specimens only half a dozen mistakes have been made. 
But the practising physician does not treat his patient statistically. 
In the individual case it is well to bear in mind the possibility of errors 
of this kind, especially in cases in which the disease does not pursue 
the course expected in some form of phthisis. 

Roentgenography.—I*rom the facts presented in Chapter XVII it is 
clear that roentgenography is of but little value in the diagnosis of 
truly incipient lesions in the lungs. Infiltrations, even when extensive, 
do not cast any characteristic shadows on the plate; the slight opacities 
they do produce are insufficient in themselves to clinch a diagnosis, or 
even to localize the active lesion, considering that there is hardly a 
chest in which opacities of various kinds, engendered by a multiplicity 
of causes, may not be seen. When the apical opacities are distinct the 
case is no more “‘incipient,’’ because they represent either caseated 
areas of lung tissue or, more commonly, fibrosis and calcification of 


1 Interstate Med. Jour., 1914, 21, 330. 


384 CHRONIC PHTHISIS, INCIPIENT STAGE 


pulmonary parenchyma and glands. But these processes, fibrosis 
and calcification, are indications of healing and may not at all be 
the cause of the symptoms. Peribronchial tuberculosis, which some 
roentgenographers describe in great detail, usually represents glandular 
fibrosis, calcification, etc., and bloodvessels, bronchi, and other struc- 
tures superimposed and crossing each other in the region of the hilum. 
While some of these opacities undoubtedly represent tuberculous 
changes, these lesions are healed, as a rule. It is commonly the 
parenchymatous lesion in the apex which gives trouble in really 
incipient cases, and these we should like to detect as early as possible, 
but they permit the rays to pass unhindered. For these reasons we 
find that the lesion, easily localized by one well versed in physical 
diagnosis, is not detected by those who rely solely on roentgen findings. 

These sad disappointments have led many clinicians of late to rely 
on the clinical aspects of the case, physical exploration of the chest, the 
history and symptomatology, etc., in their efforts at detecting tuber- 
culosis as early as possible. It has been our rule never to make a 
diagnosis of incipient tuberculosis merely because there are positive 
roentgen findings when the constitutional symptoms are not in agree- 
ment. Conversely, when the constitutional symptoms are clear cut, 
and physical exploration of the chest points to a Jesion in an apex, 
the diagnosis is unhesitatingly made even though the roentgen find- 
ings are negative, which is very often the case in instances with 
positive sputum. Exceptions are cases giving a history of several 
attacks of abortive tuberculosis, which may or may not have been diag- 
nosed at the time of their occurrence, and these attacks have left traces 
behind which reveal themselves on the plate. 

Serious errors are at times committed by those who rely solely on 
roentgen findings. A patient with sclerosis of the apex which is 
perfectly healed acquires some mild ailment which is characterized 
by cough, fever, etc., is sent to a radiographer who pronounces him 
tuberculous, and appropriate costly and prolonged treatment is 
instituted. Therapeutic pneumothorax is induced in the side of the 
chest where the opacities on the plate are more extensive and pro- 
nounced. But these opacities represent healed lesions, while the slight 
roentgen changes in the opposite side really represent the active and 
progressive lesion. The results in such cases are often disastrous. 

For these reasons no diagnosis should be made of incipient phthisis 
relying solely on the roentgen findings. Clinical observation should 
be given more attention if we are to avoid errors of omission or com- 
mission. 

The Tuberculin Tests.—The changed reactivity to tuberculin which 
is observed in organisms infected with tubercle bacilli, manifesting 
itself mainly by hypersensitiveness to that agent, has been applied 
in the diagnosis of doubtful cases, especially in sanatoriums. When first 
introduced it was heralded as specific and it was asserted that finally 
a positive and uncontrovertible test had been found which decides 
whether or not an individual is suffering from active tuberculosis. 


INCIPIENT PHTHISIS 380 


For diagnostic purposes, tuberculin is applied in various ways. It 
is introduced directly into the circulation by the subcutaneous method; 
into the lymph spaces by the cutaneous method, or applied to mucous 
membranes for normal absorption by the conjunctival method. It 
has thus been applied to the skin, mucous membrane, and subcuta- 
neously. The subcutaneous application produces general and consti- 
tutional symptoms of tuberculin intoxication, while the others, as a 
rule, produce local effects. 

Clinically the following reactions are evoked by the tuberculin 
test. 

1. A general reaction, manifesting itself after the subcutaneous injec- 
tion of tuberculin by fever, chilliness, malaise, headache, backache, etc. 





Fic. 84.—The application of the cutaneous tuberculin test. 


2. A focal reaction, consisting in congestive and inflammatory 
phenomena in the neighborhood of the tuberculous lesion. 

3. Local reactions, hyperemia and inflammatory phenomena at the 
site of the tuberculin application. Of these there are: (a) The 
cutaneous reaction of von Pirquet and several of its modifications; (b) 
mucous membrane reactions, such as the ophthalmo-reaction of Cal- 
mette and Wolff-Eisner, etc., and many others which have been dis- 
carded for valid reasons. 

The Cutaneous Tuberculin Test.—This is the simplest and unquestion- 
ably the harmless method of application of tuberculin for diagnostic 
purposes. It is usually performed on the inner surface of the fore- 
arm, though any part of the body may do; but it appears that the 
skin of the trunk is not so sensitive as that of the forearm and thigh. 

25 


386 CHRONIC PHTHISIS, INCIPIENT STAGE 


The skin is cleaned with alcohol or ether and a drop of pure tuberculin 
is applied. A suitable instrument is then used to make two abrasions, 
one about two inches away from the spot where the tuberculin has 
been applied, and the other over the tuberculin. The instrument 
devised by von Pirquet may be used. It consists of a heavy handle 
with a spade-like platinum end which is more or less sharp and used 
for the purpose of scratching or boring a cup-like depression in the 
skin. It is important that bleeding should not be caused, but only 
the superficial layer of the skin is scraped away, so as to open the 
lymph spaces and thus favor absorption of the tuberculin. A needle 
may be used for the purpose or even the point of a scalpel, making one 
or two parallel incisions through the superficial layer of the skin. I 
have found it just as effective to make the abrasion first and then 
apply the tuberculin with a toothpick, rubbing it vigorously. After 
five minutes the excess of tuberculin is wiped away with some cotton 
and the patient allowed to go without any dressing. 

If the test turns out negative, it will be seen that twenty-four hours 
later the two abrasions either heal in the same manner, or when a 
scab is formed it is of the same appearance on both abrasions. When 
positive, the control appears healed, or showing a slight scab, while 
the abrasion to which tuberculin has been applied shows an inflam- 
matory infiltration manifesting itself as a slightly elevated, red papule. 
This reaction usually appears twelve to twenty-four hours after the 
application of the tuberculin; on rare occasions it is premature, appear- 
ing within four to six hours, and may disappear soon, or remain for 
days: or it may he late in appearing; even a delay of a week has been 
observed in rare cases. 

The reaction may be slight, showing some redness with infiltration, 
or a more extensive area of redness with an appreciably raised papule. 
In some cases the red area is very extensive, simulating erysipelas, and 
the papule is very elevated. Quite often the first test results in a 
negative outcome, but a second application, about a week later, gives 
positive results. It is therefore advisable to repeat the test two or 
three times before pronouncing it unequivocally negative. 

These “secondary” reactions are usually very intense, although the 
first application was negative. It has also been noted that the tuber- 
culin sensitiveness is often increased by a second or third inoculation 
and the area at which the first inoculation was made also reacts. 
Attempts to utilize these facts for diagnostic purposes have not been 
encouraging. 

Significance of the Cutaneous Tuberculin Reaction.—Clinical experi- 
ence has shown conclusively that persons who have at any time been 
infected with tubercle bacilli react to the cutaneous tuberculin test; 
experimental investigations have confirmed it. It is immaterial 
whether the infection is followed by clinical manifestations of disease 
or not; whether the tuberculous lesion is active or quiescent, the result 
isthe same. It appears to me, however, that we do not have sufficient 


INCIPIENT PHTHISIS 387 


evidence for a conclusion as to the question how long after a lesion 
has healed does the skin remain sensitive to tuberculin. Assuming 
that no tuberculous lesion ever heals perfectly, which has not yet been 
proved, we accept that even clinically healed lesions act in this way. 

Newborn infants never react to tuberculin, but when living in 
tubercle-laden surroundings they soon show the hypersensitiveness, 
as was already shown (page 70). Inasmuch as over 90 per cent of 
humanity have been infected before reaching the twentieth year of 
life, we find that many show positive reactions to tuberculin. 

It is thus clear that for clinical purposes, when we look for evidences 
of active phthisis, this test rs of little value, because it shows not only 
those who suffer from active tuberculosis, but also such as have latent or 
healed lesions. Moreover, it is often negative in rapidly progressing pul- 
monary tuberculosis, in tuberculous meningitis, in acute miliary tuber- 
culosis and also in the terminal stages of chronic phthisis, when the 
formation of antibodies is slackened or abolished. It has also been 
found negative in the presence of other infectious diseases, like measles, 
scarlet fever, diphtheria, influenza, etc., in some cases of pneumonia, 
and often during pregnancy. In a certain number of cases of un- 
doubted phthisis the cutaneous reaction was found negative without 
any assignable reason; von Pirquet estimated it at from 2 to 4 per cent, 
but in my experience it is more than double that proportion. 

After many years of experience with this test 1t was concluded by 
most authors that a positive cutaneous reaction is of clinical value 
only in children, and that the younger the child, the more its clinical 
significance. But from more extensive experience it appears that it 
is also unreliable in children. From personal experience I am inclined 
to the conclusion that children between three and fifteen years of age 
with a positive tuberculin reaction are not necessarily doomed to develop 
active phthisis; I have even observed many infants under two years of 
age grow into healthy children in spite of the positive outcome of the 
test, and the statement of some authors to the effect that an infant 
under one year showing a positive cutaneous reaction will not survive 
a year 1s negatived by the many infants I observed and reported 
elsewhere,’ who have thrived despite the fact that during the first six 
months of their life the reaction was positive. 

Specificity of the Test.—It appears that from the scientific stand- 
point the specificity of the test has not been proved to the satisfaction of 
all, as has already been shown. Autopsy findings by Ganghofner, 
Radziejewski, Behrend, Bruckner, Retischel, and many others show 
that there are cases in which the test was positive, yet no tuberculous 
lesions were found at the autopsy, and the reverse. Experimentally 
the evidence is in the same direction (see p. 38). 

It has also been found that tuberculin is not the only substance 
capable of producing a positive skin reaction in tuberculous indi- 


1 See A Study of the Child in the Tuberculous Milieu, Arch. of Pediat., 1914, 31, 
96, 197; 1915, 32, 20, 


388 CHRONIC PHTHISIS, INCIPIENT STAGE 


viduals, but that other toxins when inoculated into the skin often pro- 
duce changes which are akin to the tuberculin reaction. Rolly’ found 
that the skin reacted when inoculated with the toxins of dysentery, 
typhoid, paratyphoid, pyocyaneus, cholera, ete. Just as with tuber- 
culin, these toxins were always negative in very young infants, and in 
children suffering from acute infectious diseases, as scarlet fever, 
measles, ete., becoming positive during convalescence. The controls, 
performed with carbol-glycerin, were always negative. In short, these 
non-tuberculous toxins showed all the characteristics of tuberculin 
when inoculated into the human skin. That any or all of these toxins 
acted in a specific manner may be ruled out because, with the excep- 
tion of tuberculosis, the individuals tested never suffered from typhoid, 
paratyphoid, cholera, diphtheria or pyocyaneous sepsis. ‘Tenzer? ob- 
tained skin reactions indistinguishable from those of the von Pirquet 
test with cholera vaccine and with a mixture of peptoalbumoses, in 
persons in whom the tuberculin test was positive. 

From these experiments, as well as from those performed by Sorgo,* 
it appears that tuberculous individuals react with a specific intensity 
to tuberculin and to other toxins, thus indicating that it is mainly due 
to hypersensitiveness of the skin. The assumption that the skin of 
the tuberculous is endowed with a specific allergy to tuberculin alone 
is thereby disproved. The allergy is evidently a cutaneous hypersen- 
sitiveness to the action of toxins in general. Hamburger,‘ one of the 
most authoritative champions of the specificity of the tuberculin 
test, after inoculating tuberculous patients with substances similar to 
those with which tuberculin is prepared (glycerin, bouillon, extractives, 
salts, ete.), became convinced that the cutaneous reaction is due more 
to the latter substances than to the tuberculin, which acts merely as a 
skin irritant. 

We are therefore justified in concluding that we are far from having 
sufficient and satisfactory information to speak with certainty about 
the cutaneous tuberculin test and its underlying causes, and from the 
theoretical standpoint its specificity has not been proved conclusively. 

However, for demographers the test is important in showing the 
wide dissemination of tuberculous infection among civilized humanity, 
though the same results could be also obtained with substances other 
than tuberculin. In children it shows whether they have been infected 
with tuberculosis, and in infants it even points to active tuberculosis; 
but in adults it 1s of no clinical value at all. 

The various modifications of the cutaneous tuberculin tests are not 
superior to the von Pirquet method. The Moro test, consisting in rub- 
bing tuberculin ointment into the skin, is of less value than the one 
described above. The percutaneous, the quantitative cutaneous test, 


Miinchen. med. Wehnschr., 1911, 58, 1285. 
Monatschr. f. Kinderheilk., 1911, 10, 131. 
Deutsch. med. Wehnschr., 1911, 37, 1015. 
Die Tuberkulose des Kindesalter, p. 37, 


a on’ 


INCIPIENT PHTHISIS 389 


etc., offer no advantages over the von Pirquet test, which is after all 
the simplest and most reliable. 

The Conjunctival Reaction.—The conjunctival reaction, invented by 
Calmette and Wolff-Eisner, is made by instilling into the conjunctiva, 
with an ordinary eye-dropper, one drop of a 1 per cent solution of 
tuberculin. The reaction appears within twelve hours and reaches 
its optimum in twenty-four hours, producing redness of the conjunctiva, 
and when the reaction is intense, the redness is more pronounced and 
there is also injection of the vessels of the eyeball and more or less 
well-marked secretion of mucus. It may last for two or three days. 
Of course, in estimating the effects of the tuberculin, comparison is 
made with the other eye. 

Among clinically non-tuberculous persons, from 10 to 25 per cent 
react, while among those who are evidently tuberculous, between 50 
and 75 per cent show a reaction with this test. It has been practically 
discarded of late because in many cases quite troublesome inflamma- 
tory phenomena appeared in the tested eye. In one of my cases the 
inflammation was so severe, persisting for three months, that I have 
ever since hesitated in applying it. Bandelier and Répke state that 
experiments on animals have shown that this test is unreliable in cases 
of human phthisis, since the reaction may be negative in spite of the 
presence of active tuberculosis unless 10 per cent solution of tuberculin 
is used, and this should not be done when dealing with human eyes. 

The Subcutaneous Tuberculin Test.—This is the test preferred by 
most of those who have confidence in the diagnostic value of tuber- 
culin in doubtful cases. It is claimed that it is not only reliable in 
deciding whether the patient bas ever been infected with tubercle 
bacilli, but also in showing whether the disease is active and that in 
many cases it even shows the area involved at the time the test is 
made by the so-called “focal reaction.” 

Of the various ways in which it is performed, the following is the 
simplest and gives the same results as any that has been devised: 

For twenty-four hours the temperature of the patient is taken every 
three hours and carefully recorded. Inquiries are made as to the 
subjective symptoms, especially pains in the chest, headache, cough, 
expectoration, ete. An injection of 0.1 mg. of tuberculin is then made 
subcutaneously in the region of the back below the angle of the scapula 
or any other place. Of course, all antiseptic precautions are to be 
rigidly observed and the skin washed with alcohol or ether. In case 
no reaction appears within forty-eight hours, a second injection is 
made with the same amount of tuberculin, while some increase it to 
1 mg. This dose is again increased in case no reaction follows to 5 
mg. and even to 10 mg. in case the test proves negative and a fourth 
injection is given. Of course, in children smaller doses are used. 

The Reaction. — Usually between ten to twelve hours, rarely between 
six to eight hours, in case the reaction is positive, constitutional, local, 
and focal symptoms make their appearance. Some say that it may 


390 CHRONIC PHTHISIS, INCIPIENT STAGE 


be delayed as long as forty-eight to seventy-two hours, but this must 
be very rare; I have never encountered it. Of the constitutional 
symptoms, fever is the most constant and reliable. The temperature 
begins to rise six to twelve hours after the injection, reaching 100° to 
102° I*., and in those showing a severe reaction, it may even go up to 
104° I*., and I have seen several cases in which it was higher. ‘There 
are usually constitutional symptoms of hyperthermia—headache, back- 
ache, pains in the joints, weakness, malaise and, in some cases, nausea 
and vomiting. Rarely the prostration is very pronounced, while in 
others it may be slight, or even absent, irrespective of the degree of 
fever. These symptoms usually subside within twenty-four to forty- 
eight hours and only rarely last longer. 

At the site of the injection the local reaction manifests itself in ten- 
derness or even pain, redness, and swelling, which may be small—only 
about 1 ecm.—but in some cases the infiltration is as large as a hen’s 
egg. Lymphangitis and enlargement of the regional lymphatic glands 
may occur. 

The so-called “focal reaction” is very rarely observed in phthisis. 
It is said to consist in congestion of the lesion in the lung, an increase 
in number and consonance of the rales, a change in the breath sounds 
and extension of the dull areas, accompanied by an increase in the 
cough and expectoration. Tubercle bacilli hitherto absent from the 
sputum may now be found. My own experience leads me to the con- 
viction that this focal reaction is very unreliable. It occurs but rarely, 
and when we recall that in phthisis the physical signs change so often, 
and that a skilful clinician one day finds signs in one side and the next 
day in another without tuberculin injections, we may always suspect 
that the focal reaction is not necessarily a result of the tuberculin 
injection; at least its inconstancy should lead us to this conclusion. 

Clinical Value of the Test.—The object of the test is to clear up doubt- 
ful cases in which there are symptoms and signs pointing to active 
phthisis but which are not convincing to clinch the diagnosis. In such 
cases the advocates of the test claim that a positive reaction decides 
in favor of active disease, while a negative outcome decisively excludes 
it. It has been used mostly in sanatoriums for these purposes. 

Careful analysis of the conditions under which this test is negative 
or positive shows that it is hardly of greater reliability than the cuta- 
neous or conjunctival test. Investigations by Franz,! Hamman and 
Wolman,? Beck,? and many others show that it may be positive in 
healthy persons who do not develop phthisis subsequently. The 
experience of all who have applied this test to large numbers of actually 
or apparently non-tuberculous individuals is the same as that of Franz, 
Hamman and Wolman, Beck, etc. Jt 1s always found that between 40 


1 Wien. klin. Wchnschr., 1909, 22, 991. 
2 Tuberculin in Diagnosis and Treatment, New York, 1912. 
3 Deutsch. med. Wehnschr., 1899, 25, 137. 


INCIPIENT PHTHISIS 391 


and 60 per cent of humanity react to the subcutaneous tuberculin test, 
providing it 1s repeated with ascending doses three or four times. 

Specificity of the Test.— We have already mentioned that many non- 
tuberculous substances have a toxic action on the organism infected 
with tubercle bacilli. Thus, according to experiments by Mettetal,! 
Preisich and Heim,? Petruschky,* and many others, nucleins, blood- 
serum, testicular extract from healthy animals, culture-free bouillon, 
and other foreign albumoses, when injected into tuberculous persons, 
may provoke reactions not unlike the general reaction of tuberculin. 
More recently the parenteral injection of milk has been found to 
produce a reaction which cannot be distinguished from that produced 
by tuberculin. It appears that the tuberculin reaction is part and 
parcel of the hypersensitiveness of the infected organism to foreign 
proteins of any kind, tuberculous and non-tuberculous (see p. 38). 

Diagnostic Value.—Considering that the subcutaneous tuberculin 
test discloses latent infection, as well as active tuberculous disease, 
its diagnostic value is limited, bearing in mind that over 90 per cent 
of humanity have been infected at some period of their lives. What 
we look for is active disease and when the test also shows those who are 
not phthisical, its value in diagnosis is limited indeed. 

“A positive tuberculin reaction,” say Hamman and Wolman, “is 
merely confirmatory evidence and never decides with certainty an 
otherwise doubtful diagnosis. Indeed we feel that caution is decidedly 
in place not to lay too much emphasis upon a positive reaction, for if 
a patient is suffering from symptoms which may be accounted for by 
a number of different conditions, and by applying the test we admit 
such uncertainty, a positive reaction does not impel the conclusion 
that these symptoms are due to tuberculosis. If such a large percent- 
age of healthy individuals harbor clinically unimportant tuberculous 
lesions, a certain proportion of those suspected of having tuberculosis 
must likewise harbor them, though the symptoms that attract our 
attention may be due to some other disease.” With this view the 
present writer agrees entirely. How far the tuberculin test has been 
discarded as a diagnostic agent is seen from the fact that in none of 
the armies engaged in the World War had it been adopted as a test 
for active tuberculous disease, though strong efforts were made to weed 
out tuberculous persons from the service. 

Dangers of the Test and Contraindications. —The subcutaneous tuber- 
culin test is not without dangers. When carelessly performed with 
excessive doses, latent or quiescent lesions may be flared up into 
activity. L. Rabinowitsch,! Bacmeister,> Leo Kessel,’ and others 
have shown that living and virulent tubercle bacilli may appear in 

1 Valeur de la tuberculine dans le diagnostic de la tuberculose de la premiere enfance, 
Thése de Paris, 1900. 

Zentralbl. f. Bakteriol., 1902, 31, 712. 
Ergebn. d. inn. Med. u. Kinderheilk., 1912, 9, 557. 


Berl. klin. Wehnschr., 1913, 1. 5 Miinchen. med. Wehnschr., 1913, 60, 343. 
Am. Jour. Med. Sci., 1915, 150, 337. 


2 
3 
4 
6 


392 CHRONIC PHTHISIS, INCIPIENT STAGE 


the blood after an injection of tuberculin. In some cases it has been 
observed that hemoptysis is provoked by the test, and all agree that 
it must not be given during, or soon after, a pulmonary hemorrhage. 
In general the reaction consists essentially in a transient toxic injury 
to the body, and the nervous system bears the brunt of the traumatism. 

It has also been found dangerous in cases of heart disease, arterio- 
sclerosis, nepbritis, diabetes, etc. In epileptics it has been observed 
that the reaction may provoke convulsions. Even Bandelier and 
Roépke say that it is contraindicated when miliary tuberculosis is sus- 
pected, “since its downward course might be accelerated.” Sahli,'! who 
uses tuberculin for therapeutic purposes extensively, says: “The use 
of tuberculin for diagnostic purposes ought to be condemned. It is 
unreliable both positively and negatively. Diagnostic injections are 
dangerous.” 

The Complement-fixation Test.—Quite recently the complement- 
fixation test on the lines of the well-known Wassermann reaction for 
syphilis has been applied in the diagnosis of tuberculosis. It has been 
studied by Besredka and Manoukhine,? Calmette and Massol,? Debains 
and Jupille' in France, and in England by James McIntosh, Paul 
Fildes,> J. A. D. Radcliffe and Edward Glover.’ In this country, 
J. Bronfenbrenner,’ A. M. Stimson,’ Charles F. Craig,? H.R. Miller, 
and others have reported good results with this test. 

But so far the results appear to be conflicting in certain points, so 
that further careful research combined with clinical observations are 
necessary before deciding on the specificity and clinical applicability 
of the test in general practice. The main difficulty is evidently the 
fact that different authors have used different antigens. Besredka 
used one prepared from egg-broth cultures of tubercle bacilli; Rad- 
cliffe used a freshly prepared unsterilized emulsion of saline solution 
of living tubercle bacilli grown on glycerin-egg medium; Hammer 
used an alcoholic extract of tuberculous tissue to which was added a 
certain amount of old tuberculin; Stimson and Bronfenbrenner use 
Besredka’s antigen; Craig’s antigen consists in an extract of several 
strains of human tubercle bacilli prepared by a special method. It 
is thus clear that with so many different methods the results are 
hardly comparable. Moreover, as McIntosh points out, Besredka’s 
antigen, cannot be considered absolutely specific since Inman and 
Kiss and Leredde and Rubinstein found that non-tuberculous syphil- 
itics gave the reaction frequently. Even if the explanation that it is 
due to the lipoids derived from the egg constituents of the medium, 


Fifth Confer. Nat. Assn. Prev. Consumption, London, 1913, p. 57. 

Ann. de l’Inst. Pasteur, 1914, 28, 569; Compt. rend. Soe. de biol., 1914, 76, 197. 
Ibid., 28, 338. 

Compt. rend. Soe. de Biol., 1914, 76, 199. 

Lancet, 1914, 2, 485. 6 Quarterly Jour. of Med., 1915, 8, 339. 
Arch. Int. Med., 1914, 14, 786; Proc. Soc. Exper. Biol. and Med., 1914, 12, 48. 
Bull..101, Hyg. Laborat., U. S. P. H. 8., 1915. 

Am. Jour. Med. Sci., 1915, 150, 781. 


oon et pep wre we 


INCIPIENT PHTHISIS 393 


which react with the syphilitic serum in a manner similar to tissue- 
extract antigen, is correct, it does not help us in our efforts to find a 
specific test for active tuberculosis. 

Various authors report between 40 and 95 per cent of positive 
results with the complement-fixation test. Some state that a positive 
reaction means an active tuberculous process somewhere in the body. 
McIntosh and Fildes state even that a small lesion may not reveal 
itself by this test: ‘The lesion must be of considerable dimensions 
before the reaction can detect it. A caseous bronchial gland will not 
give a positive reaction; indeed, the common affection of the cervical 
glands will usually yield a negative result. On the whole, we have 
come to the conclusion that a lesion in order to give positive results 
must be of such dimensions as to constitute ‘disease’ and require the 
intervention of the physician or surgeon. We look upon the positive 
reaction, therefore, as indicating ‘active tuberculosis.’ ’’ On the other 
hand, Craig found that 65 per cent of clinically inactive cases of pul- 
monary tuberculosis gave positive reactions. Most writers obtained 
positive reactions in patients with syphilis. 

This test has been given an extensive and careful trial in my wards 
at the Montefiore Hospital. My associate, Dr. H. R. Miller, has 
applied it in a very large number of cases. But I have not been 
impressed with its reliability as a diagnostic agent when we attempt to 
discriminate between tuberculous infection on the one hand and active 
tuberculous disease on the other. In many active cases it has been 
negative, while many non-tuberculous cases showed positive results. 
It appears to be of about the same value as the von Pirquet skin reac- 
tion. It, as arule, discloses infection. To discover infection, the skin 
reaction may be applied with less trouble. 

The Autourine and Autoserum Test.—The search for a biochemical 
test for active tuberculous disease has recently brought forward another 
reaction. Wildbolz! believes that he has discovered that when a 
tuberculous process is active in any part of the body the urine contains 
an antigen which produces circumscribed redness and infiltration when 
injected intradermally by the Mantoux method. He reported that 
urine from healthy individuals, when injected into the skin of tubercu- 
lous patients, does not produce this reaction, nor do healthy persons, 
or even tuberculous patients but in whom the lesions have healed, 
eliminate this antigen with the urine. Moreover, he found that the 
reaction goes hand-in-hand with the tuberculin reaction; the response 
is positive when the tuberculin test is positive, and the reverse. His 
conclusion is that the urine in tuberculous patients eliminates specific 
substances akin to those contained in tuberculin, and that they may be 
utilized for diagnostic purposes when the problem is whether the 
disease is active or healed. 

As a rule, the morning urine is used. It is evaporated in a vacuum 


1 Cor.-Bl. f. Schweiz. Aertze, 1919, 49, 793. 


394 CHRONIC PHTHISIS, INCIPIENT STAGE 


to one-tenth its volume, and after it is cooled it is passed once or twice 
through a paper filter impreganted with a 2 per cent solution of carbolic 
acid. He found that no results are obtained with unconcentrated 
urine, while when concentrated at a high temperature on an open water- 
bath the reaction is but weakly positive. Wildbolz makes three 
sets of inoculations at an interval of 2 to 4 cm. on the arm. Two 
inoculations are made with the concentrated urine, two with 1 to 1000 
tuberculin, and two with 1 to 10,000 tuberculin. When the test turns 
out positive, the infiltration and redness are of the same degree at each 
point of inoculation. The only difference to be noted is that the 
tuberculin reaction persists for some time, while the urine reaction is 
evanescent and fades away completely within one or two days. Wild- 
bolz,! and Imhof? found that the antigen is not only found in the urine, 
but also in the blood serum which has been freed from its proteins. 
This could be expected considering that the antigens are brought from 
the tuberculous lesion to the organs of excretion, the kidneys, by the 
blood stream. Imhof found that the autoserum reaction is, as a rule, 
slightly weaker than the autourine reaction, but while in the latter 
necrosis occurs at times at the point of inoculation, this never occurs 
with the autoserum reaction. 

Clinical tests made by various authors have not altogether sustained 
Wildbolz’s experiences. Some authors report that it is of value in 
differentiating active tuberculosis because healed and encapsulated 
lesions do not respond. ‘This has been reported to be the case by 
Lanz,* Cepulic,* Alexander,’ Cole B. Gibson and William E. Carroll® 
in this country, and others. 

More intensive study has, however, shown that this test is of no 
more clinical value than the tuberculin tests. Trenkel’ is inclined to 
the idea that the reaction is not of a biological nature, but purely 
chemical. He found that in moribund patients, in whom the tuberculin 
test was negative, the autourine test was positive. He also found that 
when a specimen of urine was partly concentrated in a vacuum, as 
directed by Wildbolz, and partly in an Erlenmeyer flask without a 
vacuum, necessitating a higher temperature for evaporation due to its 
being carried out at atmospheric pressure, the results obtained were 
the same in each case, though the high temperature in the Erlenmeyer 
flask has undoubtedly an effect on the thermolabile constituents of the 
toxins. [or this reason he is inclined to attribute the reaction occurring 
on the skin to the salts of the urine and not to its toxin contents. 
Moreover, he obtained positive results with an “artificial urine.” 
Alexander found that urine containing staphylococci also gives a posi- 


1 La Presse médicale, 1920, p. 782. 

2 Schweitz. med. Wehnschr., 1920, 50, 1033. 
3 Schweitz. med. Wchnschr., 1920, 50, 321. 

4 Beitr. z. Klin. d. Tuberkul., 1921, 46, 435. 
5 Ztschr. f. Tuberkul., 1921, 33, 321. 

6 Jour. Am. Med. Assn., 1921, 76, 1381. 

i Beitr. z. Klin. d. Tuberkul., 1921, 47, 219. 


INCIPIENT PHTHISIS 395 


tive reaction. Weisz! applying fractional analysis to the urine, failed 
to discover any specific antigens corresponding to those found in 
tuberculin, and he concludes that this method is of no value in dif- 
ferentiating active from latent tuberculous lesions. Gramen,? Elias- 
berg and Schiff,’ Reinecke,‘ and many others, have found that clinically 
the test does not work out. Many non-tuberculous persons give posi- 
tive reactions, and the reverse. Finally, Farrago and Randt® found 
that patients react to urine voided by persons who showed not the 
slightest evidences of clinical tuberculosis, such as physicians, nurses, 
orderlies, and hospital patients suffering from slight ailments. Their 
conclusion is that the reaction is of traumatic and chemical origin 
and not specific, and for these reasons cannot be considered of diagnostic 
value. j 

Other Special Tests.—Most of the other special diagnostic tests 
which have been brought forward from time to time have been found 
wanting in reliability; their limitations preclude their general adop- 
tion. Arneth’s blood-picture has never been considered of diagnostic 
value and was only urged as of prognostic significance (see p. 244). 
Wright’s opsonic-index method has been given a very extensive trial, 
especially in English-speaking countries, but has been found unreliable. 
The results are very conflicting and the method is altogether unsuit- 
able for general adoption. 


1 Med. Klinik, 1921, 17, 950. 

2 Hygeia, 1920, 82, 674. 

3 Monatschr., f. Kinderheilkunde, 1920, 19, p. 1. 
4 Miinchen. med. Wehnschr., 1920, 67, 1202. 

5 Deutsch. med. Wehnschr., 1921, 47, 919. 


CHAPTER XX. 
CHRONIC PHTHISIS, ADVANCED STAGE. 


Duration of the Incipient Stage.—Incipient phthisis is also called 
“early” phthisis, and thus confusion is engendered in the minds of the 
laity, as well as of physicians, who assume that a case is incipient only 
for a certain time and then progresses to the second or third stage, 
unless properly treated. This is wrong. There are cases which are 
“advanced” soon after the active symptoms manifest thsemselves, while 
others, though remaining active for years, never pass beyond the stage 
of inciprency. Indeed, we meet with numerous patients who have been 
tuberculous for many years, and have been admitted to sanatoriums 
several times as “early”’ cases. 

The sagacious clinician Laennec, stated nearly one hundred years 
ago that it appeared to him that hardly any consumptive succumbs to 
the first attack of the disease, and that in the vast majority of cases 
the first attack is erroneously diagnosticated as a mild respiratory 
trouble. The disease then remains latent for a longer or shorter time 
to break out again, perhaps with greater severity. Many years of 
research along scientific lines have confirmed Laennec’s observation. 
A large number of cases never become “advanced” in the sense we use 
this term. Others show greater activity, and the process in the lungs 
proceeds from infiltration to caseation, softening and excavation within 
six months or a year. A large proportion of active cases remain 
quiescent for one or two years, and then suddenly take a turn for the 
worse and the patient sinks, succumbing to exhaustion, or to some 
complication. 

On the whole it may be stated that in the clinical sense, “inciprency”’ 
does not necessarily imply earliness of the process. As used by physicians 
and understood by patients, it means a limited and circumscribed 
lesion which is not manifesting a tendency to acute progression, but 
either remains quiescent or leans to cicatrization of the lesion. In 
this stage the patient may remain for many years and no average 
duration can be assigned. It can only be estimated in the individual 
patient, depending as it does on so many different and complex factors 
which have been discussed elsewhere in this book. 

Course of Incipient Phthisis.—In a large proportion of cases phthisis 
does not pass beyond the so-called stage of incipiency. The patient 
coughs, expectorates, has fever, hemoptysis, etc., for several weeks or 
months, and, after taking a rest in the country, spending a few months 
in a sanatorium, or even while continuing at his occupation, he slowly 


OSCILLATING COURSE OF CHRONIC PHTHISIS 397 


recuperates and recovers, never to be troubled again with pulmonary 
symptoms. In most of these cases there are left remnants of the pul- 
monary lesion in an apex, manifesting themselves in impaired resonance, 
prolonged expiration and sibilation. This conforms to the abortive 
type of tuberculosis which will be discussed later on (Chapter X XI). 

But in many cases the disease progresses steadily, especially when 
no proper treatment has been instituted, and occasionally irrespective 
of the treatment. Ina small proportion of cases the progress is rather 
rapid, and within one or two months after the first symptoms have 
appeared, the patient is a confirmed consumptive; while in others the 
course is slower, the patient keeps on coughing, expectorating, losing 
flesh and strength for several months or years, when a change takes 
place and he is apparently improved or cured, or he succumbs to the 
disease. 

In the vast majority the progress of the disease is marked by dis- 
tinct remissions, during which the patient feels comparatively well, 
is able to pursue his vocation, and he, as well as his physician, is 
under the impression that a permanent cure has been attained, to be 
undeceived, now and then, by the appearance of an acute exacerbation 
of the disease during which the patient is laid up for several days or 
weeks, or by a pulmonary hemorrhage, which may or may not be 
copious; an attack of pleurisy, with or without effusion, etc. 

There is another class of cases in which the focus in the lung remains 
quiescent, but does not cicatrize for many years. Physical examina- 
tion of the chest shows distinct signs of an active pulmonary lesion 
and an examination of the sputum may even disclose tubercle bacilli, 
but the symptomatology and course are benign—the cough is mild, 
there is no fever, no nightsweats, no emaciation, and the patient is 
capable of working at his vocation for years. These may be considered 
“carriers.” ‘Though harboring tubercle bacilli in their lungs, and 
disseminating them with the sputum, they are themselves fairly 
healthy. 

Oscillating Course of Chronic Phthisis.—<A continuous course from 
bad to worse till the patient dies, or with improvement till he recovers, is 
uncommon in chrone phthisis. It is characteristic of either the abortive 
form of phthisis, on the one hand, or of acute galloping phthisis, on the 
other. But the usual case of chronic phthisis pursues a discontinuous, 
paroxysmal, I may say a capricious course, marked by periods of acute 
or subacute exacerbations of the symptoms, and periods of remissions 
during which the patient 1s more or less free from the troublesome symp- 
toms, or he may even feel comparatively well, working efficiently, 
especially if he is engaged in some intellectual pursuit. I have seen 
many who have worked at hard manual labor for months until an — 
acute exacerbation laid them up for several weeks, but they sooner or 
later recuperated and went to work again, until another acute exacer- 
bation interfered. 

These acute exacerbations during the course of chronic phthisis 


398 CHRONIC PHTHISIS, ADVANCED STAGE 


usually have distinct pathological substrata. In active phthisis the 
affected part of the lung caseates, softens and is finally eliminated by 
cough and expectoration, leaving a fistula to drain the excavation, 
which is surrounded by a fibrous capsule that inhibits or prevents 
absorption of toxic matter. The patient may feel comparatively well 
so long as the cavity in the lung is well drained. But now and then the 
fistula is obstructed, or a new area becomes involved by contiguity or 
metastasis, and again acute symptoms of constitutional toxemia make 
their appearance. This acute exacerbation keeps on for some time till 
either the fistula opens again, or the newly involved area has softened, 
the products of tissue disintegration are eliminated, and the patient 
feels well again, though he is by no means cured. 

This undulating course of phthisis can be clearly observed by study- 
ing the temperature, expectoration, emaciation, etc., of the patients, 
as was done by Bezancon,! Serbonnes,? and others. It may keep on 
for many years. In most cases one of two things finally occurs—either 
the infiltrated or excavated area in the lung cicatrizes, or becomes 
encapsulated and shrinks and the disease is arrested; or, during one 
of these exacerbations, the pulmonary involvement becomes too 
extensive, and can no more become quiescent and, with or without 
some complication, the patient succumbs. 

We may say that during the long course of chronic phthisis there is 
an intense struggle between the bacilli and the resistance of the host. 
We have seen that everybody possesses more or less resistance; else 
every infection would speedily prove fatal. In this struggle the bacilli 
gain the upper hand for a time and cause an acute exacerbation, but 
the innate resistance is again called upon and usually responds, the 
result being a truce, until the bacilli again catch the organism napping. 
The final outcome depends on many and complex factors which are 
discussed elsewhere. 

Symptoms.—The cough, which may have been mild during the 
incipient stage, gr adually becomes more and more annoying and 
productive. It may be painful, paroxysmal and exhausting, and end 
in vomiting, especially after the evening meal. But with the advance 
of the process the cough is ameliorated in most cases; while it does 
not cease altogether, it becomes “looser”; the sputum is brought up 
without great effort. During acute exacerbations it is usually aggra- 
vated, often painful, due to complicating dry or moist pleurisy, etc. In 
some cases the cough is mild throughout the course of the disease, while 
in others it constitutes the main complaint of the patient. In fatal 
cases it may be absent during the last few days of life, when the reflexes 

_are abolished, or, because of severe emaciation and muscular atrophy, 
the patient has not enough strength for the efforts at coughing. 

The mucoid sputum of the incipient stage becomes more and more 
mucopurulent with the advance of the disease, and almost invariably 


1 Paris médical, 1911, p. 133. 
> Les Poussees évolutives de la tuberculose pulmonaire chronique, Paris, 1910. 


SYMPTOMS 399 


contains tubercle bacilli. Exceptionally, none are found in a case 
that keeps on progressing, even toa fatal issue. But this is exceedingly 
rare. Elastic fibers are, however, found in practically all cases in which 
the disease has passed incipiency, owing to the destruction of lung tissue 
during caseation and liquefaction. Immediately before and during an 
acute exacerbation the amount of sputum may be diminished, but 
within a few days it again increases in quantity. With the disinte- 
gration of lung tissue and formation of vomice, the character of the 
sputum changes; it becomes thick, nummular and sinks in the water 
of the receiving vessel. During hemorrhages it is sanguineous, and 
often without any evident hemorrhage it is tinged with blood. During 
quiescent periods the amount expectorated is, as a rule, diminished; it 
may lose its purulent character and, when a cure is established, the 
expectoration may cease. In fatal cases we often note that during the 
last few days little sputum is brought up. The patient has not suffi- 
cient strength to expel it, as has already been mentioned. 

The temperature in active advanced cases is not of a characteristic 
type. In progressive cases it may be continuous or remittent till 
the end—recovery or death. Usually the curve, when studied for 
several months continuously, pursues an undulating or cyclic course. 
For several weeks it is high, no matter what type it is, rising to 101°, 
or even 104° I. in the afternoon, and declining several degrees in the 
morning, im many cases even to a subnormal degree. Slowly an 
improvement is noted, the temperature becomes lower and lower and 
we may find a period of either subfebrile or even normal temperature 
for a few weeks. In many cases I have noted a subnormal tempera- 
ture for comparatively long periods. 

But suddenly—perhaps after a chill or some indiscretion—or grad- 
ually, the temperature rises again and keeps at a high level for several 
days or weeks, thus marking an extension of the process to a hitherto 
unaffected area of the lung, or some complication. 

It is noteworthy that, asa rule, during the afebrile periods the patient 
feels quite well and, for weeks, may consider himself cured, to be sadly 
disappointed during the acute exacerbations which are sure to come in 
most cases. Even during febrile periods many feel comparatively 
well and have a good or fair appetite, as was already stated. The 
intellect is usually clear; those engaged in intellectual pursuits may 
follow their vocations during the exacerbations. I have had patients 
who did business on a high scale under such circumstances, and writers 
and artists who produced their best work while the thermometer 
registered 103° F. The euphoria, which is characteristic of phthisis, is 
best observed in far-advanced cases. 

Emaciation goes hand-in-hand with other constitutional symptoms, 
especially fever. Those who have no quiescent periods lose flesh very 
rapidly, and within a few months may be reduced to mere skeletons. 
In those in whom the disease runs an undulating course, we often 
note a gain in weight during afebrile periods, and if the fever is mild 


400 CHRONIC PHTHISIS, ADVANCED STAGE 


durmg acute exacerbations and of short duration, the loss in weight 
may \be insignificant. They may be ahead in this regard at the end 
of a year or two, although the process in the lungs remained stationary, 
or has even progressed. 

Toward the end the emaciation is very pronounced and deserves 
the name consumption. Then it is not only the fever, cough, and 
expectoration that are exhausting the patient, but also the lack of 
nourishment owing to anorexia, diarrhea, and perhaps dysphagia when 
the larynx is implicated. The preservation of the body weight, which 
is very frequent in fibroid phthisis, is only rarely seen in chronic 
progressive phthisis, and, when found, it is an indication of improve- 
ment, or that the quiescent periods are of long duration. 

Hemoptysis is comparatively infrequent during this period, except- 
ing in very advanced cases with cavities, when a terminal hemorrhage 
may carry off the patient, and in those suffering from hemorrhagic 
phthisis (see p. 240) it may recur at irregular intervals. As was 
already stated, most of the hemorrhages at this period, even when 
profuse, end in recovery. 

The other symptoms of chronic phthisis have already been described 
in detail in previous chapters. 

Physical Signs.—Depending on alterations in the pulmonary 
parenchyma, pleura, mediastinum and chest walls, the physical signs 
of advanced phthisis are complex. By percussion and auscultation 
we may determine, with a reasonable degree of certainty, the nature 
of the lesion, as well as the condition of the apparently unaffected 
parts of the thoracic viscera. But with the progress of the disease, 
the changes found on physical exploration become more and more 
variegated and, owing to frequent overlapping of pathological changes, 
their complexity is so great that it is often quite difficult or impossible 
to determine exactly the details of these changes by physical examina- 
tion. This is well illustrated by the difficulties encountered while 
attempting to determine the presence or absence of pleural adhesions 
before inducing a therapeutic pneumothorax and by the number of 
cavities that are missed during life and found at necropsy. Roentgen- 
ography is of immense value at this stage, but it is not infallible, as has 
already been shown. 

Percussion.—The tuberculous infiltration usually extends in hori- 
zontal planes; metastatic deposits of tubercle at a distance from the 
original focus in the same or the opposite lung are only rarely found. 
The result is that the impairment of resonance found over one apex 
during the incipient stage extends mainly downward, and, in progres- 
sive cases, we soon find dulness as far as the third or fourth rib, or lower. 
The pitch of the note depends on the density of the infiltration, on the 
presence or absence of excavations, the amount of secretions in the 
cavity, and on the condition of the pleura. On the unaffected side a 
hyperresonant note may be elicited, which may be accentuated by 
vicarious emphysema. 


AUSCULTATION 401 


Dulness is very frequently found in the interscapular spaces, which 
may be an expression of enlarged peribronchial glands, or infiltration 
of the apex of the lower lobe of the lung. In the majority of cases 
there is more or less retraction of the base of the lung, easily made 
out by tidal percussion. 

With percussion we may also determine the position of the heart 
which in many cases is of immense diagnostic significance, as has 
been pointed out elsewhere by the writer.!. In phthisis the heart is, 
as a rule, dislocated toward the affected side, the reverse of conditions 
found in pleural effusions, pneumothorax, intrathoracic neoplasms, 
etc. It is therefore important to determine the position of the heart 
in cases showing intense dulness of the lower parts of the chest on one 
side when the problem arises whether it is due to an effusion, or to 
thickened pleura with pulmonary retraction. Exploratory puncture, 
if negative, is not conclusive, but when we find the heart displaced to 
the opposite side, we may conclude that there is an effusion, while 
when it is dislocated toward the affected side, it is due to excavation 
and to pleural thickening. But to this there are many exceptions 
which are discussed elsewhere. 

The routine methods of physical exploration show the location of 
the heart in phthisis easily and vividly; but in many cases the diag- 
nosis js difficult and occasionally almost impossible. The side of the 
heart adjoining the healthy lung is easily made out by percussion, but 
the cardiac dulness at the side adjoining the affected lung merges 
with the dulness of the infiltrated and consolidated lung tissue or thick- 
ened pleura, and it is difficult to separate by any method of percussion. 
The fluoroscope and the roentgenographic plate also fail at times to 
show a definite outline of the borders between the heart and the lung. 
Indeed, I have found at times that orthodiagraphy was of no avail. 

Dextrocardia is not rare in extensive right-sided lesions. It is to be 
differentiated from complete transposition of the viscera by the loca- 
tion of the liver, spleen, etc. 

Auscultation.—Auscultation in advanced phthisis is of even greater 
diagnostic significance than percussion and roentgenography, because 
it shows distinctly the progress of the process in the lungs, especially 
its activity. The diagnosis of a healed lesion can only be made by a 
study of the constitutional symptoms, and a careful consideration of 
the auscultatory phenomena elicited over the chest. 

The breath sounds which, during the incipient stage, may have been 
somewhat altered, rough, cog-wheel or feeble, now become more and 
more bronchial or tubular in character. Excepting in very acute cases, 
which do not concern us here, bronchial breathing does not appear 
suddenly in chronic phthisis. Following a progressive case we may 
observe that the cog-wheel breathing changes by degrees; first the 
expiratory murmur becomes prolonged, then the sounds assume a 


1 Arch. Int. Med., 1914, 13, 656. 
26 


402 CHRONIC PHTHISIS, ADVANCED STAGE 


bronchovesicular character, indicating that the breath sounds are 
mixed, the vesicular coming from the healthy lung and the bronchial 
from the disseminated infiltrated patches. When these patches con- 
glomerate, and the part of the lung consolidates into an extensive 
airless area, thus acting as a good conductor of the laryngo-tracheal 
murmur to the surface, we get bronchial breathing. With the onset 
of softening the products of tissue disintegration are expelled, leaving 
an excavation and we often, though not invariably, hear cavernous 
or amphoric breathing, which will be discussed later on. 

The advance of the lesion is characterized pathologically by soften- 
ing of lung tissue, followed by liquefaction and cavity formation. 
These changes are best determined by auscultation and the detection 
of moist rales which are produced by the air current passing from 
the bronchi into the diseased area filled with morbid secretions and 
débris of disintegrated tissue. These rales are of various sizes—large, 
medium or small—according to the size of the bronchus, or the excava- 
tion in which they are produced. Usually they are consonating, 
ringing and either provoked, or intensified, by cough. Their diagnostic 
significance lies in their localization and persistence. They are mostly 
found over the supraspinous fosse, in the upper part of the interscapu- 
lar space, and especially above and below the clavicle, and with them 
we usually hear low-pitched, bronchial breathing. When heard uni- 
laterally and persistently in any of these locations, they are, with but 
few exceptions, pathognomonic. 

The onset of softening is characterized by the appearance of moist 
rales, usually small or of medium size. They have been called by the 
French rdles de friture because they simulate the sounds heard when 
frying something. But we must guard against overestimating the 
extent of the disease by wide distribution of rales. With concomitant 
bronchitis they may be distributed all over the chest, or all over one 
hemothorax, while the tuberculous lesion is rather limited. After 
pulmonary hemorrhages rales may be heard far away from the tuber- 
culous area, and we must be guarded 1n concluding that it is an indica- 
tion of widespread extension of the tuberculous lesion. The thermom- 
eter is a better guide under such circumstances. After an attack 
of influenza there may remain a large number of rales which dis- 
appear in time. 

On the whole, it can be stated that the activity of the tuberculous 
process may be gauged by the number, character, and distribution of 
moist rales audible over the chest. The larger their number, the larger 
their consonance, when localized over a limited area, the more active 
the process, while absence of rales indicates an arrest in the progress of 
the disease. All this is true when, in addition to these adventitious 
sounds, there are also constitutional symptoms, especially fever. 
In the absence of toxic symptoms, rales may be heard in chests with 
quiescent, or even arrested tuberculous disease. 

Sibilation is quite frequently heard in cases of advanced phthisis 


CAVITIES 403 


and it may be caused by various conditions. In the interscapular 
spaces, and near the two sides of the sternum, whistling sounds are 
an indication of tracheo-bronchial adenopathy with pressure on the 
bronchi. In some cases, we hear sonorous rales all over the chest, or 
unilaterally, in cases complicating bronchitis or emphysema; over 
areas of localized vicarious emphysema, sibilation is also heard at 
times. [ora long time, or permanently after a lesion has healed, there 
may remain sibilation, “cicatricial rales.”’ 

Friction sounds are very frequently heard. Their significance is 
discussed in connection with pleurisy. 

Cavities. —This stage is characterized by the formation of pulmonary 
excavations. ‘The constitutional symptoms accompanying the forma- 
tion of cavities depend on the acuteness of the process. So long as 
the excavation is surrounded by infiltrated and caseated lung tissue, 
the symptoms are acute—high fever of a continuous, or remittent 
type, profuse nightsweats, severe cough with abundant expectoration, 
rapidly progressing emaciation, etc. But in most cases the process 
is not so acute. The excavation is surrounded by a fibrous shell which 
limits its progress, and prevents absorption of the toxic products to 
a great extent, so that the patient may feel quite well despite the 
formation of more or less extensive excavations in his lungs. In the 
chronic cases that do not succumb, but do not heal either, the cavity 
may keep on secreting mucopurulent matter which is promptly 
removed through the fistulous tract that leads to a bronchus. 

It is in these chronic cavitary cases that we meet the undulating 
clinical picture of phthisis described above. Whenever the fistulous 
tract leading from the cavity is obstructed, the amount of expectora- 
tion is diminished and fever, nightsweats, etc., result, till the plug in 
the bronchus is dislodged, when expectoration begins to drain the 
cavity and the patient again feels comparatively well. 

Diagnosis of Cavity in the Lung.—If we should accept the signs given 
in text-books as infallible criteria, the diagnosis of cavities is very 
simple. But those who often make autopsies and have opportunities 
to verify their findings are frequently amazed at the large number of 
cavities found intra vitam, but missing at the autopsy, and the reverse. 

In order that a cavity should be discerned by physical explora- 
tion, or even by roentgenography, it must attain the size of at least four 
centimeters in diameter; it must be superficially located, filled with 
more air than secretions and communicate with a bronchus. In the 
apex cavities are often missed because the thick, indurated pleura 
screens all signs. Some even maintain that they must have smooth 
walls if we are to elicit by auscultation and percussion the signs which 
are characteristic of excavations. In fact, many authors who have 
studied the physical signs of vomice, verifying their findings at 
necropsies, found that many excavations are overlooked, while others 
that are diagnosed are not found at the autopsy. For this reason some 
believe that the presence of elastic tissue in the sputum is the best sign 
of pulmonary excavation. 


404 CHRONIC PHTHISIS, ADVANCED STAGE 


Inspection aiid palpation are of little value. The muscular atrophy 
noted over deep excavations above and below the clavicle may be 
seen in pulmonary retraction without excavation. Over superficial 
cavities, extreme atrophy of muscles and integuments of the area 
overlying the excavations is very frequent. This atrophy leaves the 
chest wall over a circumscribed area very thin and, combined with 
pleural adhesions and retraction, may cause a cup-shaped depression 
localized over the site of the cavity, which is pulled in during inspira- 
tion. But this is comparatively uncommon, probably because many 
cavities are situated deeply within the lung. 

Percussion over a cavity gives a dull note, and only over large exca- 
vations, superficially located in the infraclavicular region of emaciated 
patients, and filled mostly with air, may be obtained a hyperresonant 
or tympanitic note. At most, we usually find dulness with tympanitic 
overnote. But to indicate excavation, even this must be strictly 
localized and circumscribed. The resonance may change within a 
single day from tympany to dulness when it fills up with secretions. 
From the roentgenograms on Plate XVII it will be seen that percussion 
of this chest would have elicited a dull or flat note one day, while the 
next, it would have been hyperresonant or tympanitic. 

On the whole, cawty tympany depends on many factors. In young 
persons, with elastic and resilient chest walls, it is more often present 
over small excavations than in the aged, whose chests are usually 
rigid and unyielding, and even large excavations may not be tympanitic. 
The more superficial the location, the more pronounced the tympany, 
while deeply lying cavities are screened by air containing lung tissue 
and tympany is altogether absent. It is thus evident that tympany 
is not a constant sign of cavitation, but when localized, circumscribed and 
pronounced it speaks for a cavity of large size with greatly relaxed 
walls; and conversely, we find high tympany over tight walls of small 
cavities. It may best be perceived, as Flint showed long ago, when the 
ear is close to the patient’s mouth, or when the bell of the stethoscope 
is held in this position. Cracked-pot resonance is also best perceived 
in this manner. 

The most common site of tympany due to cavitation is above the 
fourth rib anteriorly, and on rare occasions we find it in the axillary 
line beneath the fifth rib, especially in the left side, while posteriorly 
it is exceedingly rare because of the large muscles which interfere with 
percussion. I have met with cavities that were tympanitic over three- 
fourths of the chest wall, indicating excavation of almost an entire 
lung. But this is rare because in such cases the mediastinum is pulled 
over and produces dulness. 

Occasionally the tone changes known as Wintrich’s, Friedreich’s and 
Gerhardt’s phenomena are of assistance in the diagnosis of vomice, 
but not so frequently as some text-books would lead us to believe. 

Wintrich’s phenomenon, obtained by percussion while the patient 
opens and closes his mouth, the note being tympanitic when it is 


DIAGNOSIS OF CAVITY IN THE LUNG 405 


open, and of lower and deeper pitch when closed, is a good indication 
of a cavity communicating with a bronchus and is more distinct the 
greater the diameter of the bronchus. It may be obtainable only in 
certain positions of the body (interrupted Wintrich), which is clearly 
due to the presence of fluid secretions within the cavity which obstruct 
the opening of the bronchus. It is also met with in some cases of 
bronchiectatic excavations, but this is to be distinguished by the 
location of the cavity—anteriorly and above in tuberculosis, and 
posteriorly and below in bronchiectasis. It may also be found in 
pneumothorax, but the concomitant symptoms and signs clear up 
the diagnosis, excepting in the localized and latent forms, which can 
only be recognized with the x-rays. 


Gerhardt’s phenomenon 1 






Stethoscope } 


x 
Interrupted Wintrich’s 
phenomenon 




































































Biermer’s phenomenon; 
coin-percussion 


= shaded = fluid 
Clear space = air 


Fiag. 85.—TIllustrating Gerhardt’s and Biermer’s phenomena, interrupted Wintrich’s 
phenomenon and coin-percussion. (Musser.) 


William’s tracheal tone, observed while percussing the consolidated 
apex which conducts the tracheal tympany, is at times mistaken for 
Wintrich’s phenomenon. It is usually found in cases of contraction 
or consolidation of lung tissue, or its compression in pleuritic exudates, 
when percussion above and below the clavicle sets up vibrations in 
the main bronchus and the trachea. 

Friedreich's phenomenon consists in high-pitched tympany over the 
site of excavations when the patient holds his breath during full inspira- 
tion, diminishing during extreme and held expiration. This is not so 
reliable as Wintrich’s sign because it is at times obtained over healthy 
lungs. 


406 CHRONIC PHTHISIS, ADVANCED STAGE 


In Gerhardt’s phenomenon the note is higher and more tympanitic 
when the patient is sitting or standing than when he is reclining, and 
is said to be characteristic of an oval-shaped cavity filled partly 
with fluid and partly with air, the fluid gravitating according to the 
position of the patient. Small cavities, superficially located, occasion- 
ally show this sign and when the excavation is centrally located, it 
must attain considerable dimensions to be thus characterized. As 
Sahli points out, Gerhardt’s phenomenon is rare, and slight differences 
in the percussion note with changes in position may be within physio- 
logical limits due simply to alteration in the tension of the thoracic 
walls without any cavity within the chest. 


Interrupted ; 
Gerhardt’s Wintrich’s Biermer’s 
phenomenon phenomenon phenomenon 


VY 





































SS £55 Se we Meee 


Rn << ae ae = 


Fig. 86.—Illustrating Gerhardt’s and Biermer’s phenomena and interrupted 
Wintrich’s phenomenon. (Musser.) 





In hydropneumothorax we often observe Biermer’s phenomenon, 
which is produced in the same manner as Gerhardt’s in pulmonary 
cavities (see Figs. 85 and 86). This shifting of fluid in pneumothorax 
is discussed more fully in another portion of this book (see Chapter 
XXVII). 

Cracked-pot resonance, first described by Laennec, is occasionally 
obtained over cavities. Some precautions are necessary in order to 
elicit this sign. The patient should keep his mouth wide open, the 
pleximeter finger placed over the second or third intercostal space 
anteriorly, and with the percussion finger a strong blow is delivered 
without rebound, at the end of expiration. It is apparently a stenotic 
murmur at the opening of the cavity into a bronchus when the air is 
suddenly expelled through a narrow, slit-like opening. Plesch’ says 
that for the production of the cracked-pot resonance the cavity must 
be surrounded by elastic tissue which helps in producing a double 
motion of the air—a sudden expulsion from and quickly sucking it 
back into the cavity. It is imperative that the two pleural sheets 
overlying the cavity should be adherent and the thorax should be 


1 Deutsch. med. Wehnschr., 1917, 43, 175. 


CAVERNOUS AND AMPHORIC BREATHING 407 


resilient and elastic. It may, however, be met with in many other 
conditions, as in a crying child, and in adults with relaxed lungs, also 
in emaciated persons with resilient chest walls, and in cases of small 
emphysematous islands surrounded by consolidated lung tissue which 
are not uncommon in chronic phthisis. Of the many cavities that 
I have seen, cracked-pot resonance was present in but a small propor- 
tion. When obtained in connection with some of the other signs it 
is of significance. 

Cavernous and Amphoric Breathing.—Auscultation may be altogether 
negative over deeply lying vomice, or such as are completely closed 
by a plug in the communicating bronchus. Cavernous breathing is 
often heard; it resembles the sound produced while blowing into an 
inclosed hollow space. It is caused by the overtones developed in the 
cavity by reflection from the walls. Over cavities having smooth 
walls communicating with a bronchus we often hear amphoric breath- 
ing—a murmur with high overtones lacking deep basal tones, resem- 
bling the sound produced by blowing across the opening of a narrow- 
mouthed vase. Cavernous and amphoric breathing have a certain 
diagnostic significance. ‘They indicate pulmonary excavation, bronchi- 
ectasis, or pneumothorax. Formerly it was thought that pneumo- 
thorax shows amphoric breathing only when it is freely communicating 
with a bronchus. But now we often find it over artificial pneumo- 
thorax, and it is then due to reverberation of the bronchial sounds 
from the smooth pleura. Over many excavations only loud and harsh 
bronchial breathing is audible. 

Over areas with amphoric breathing we usually elicit a dull note on 
percussion and, at times, cracked-pot resonance, while over areas 
with cavernous breathing we often get tympanitic resonance, though 
not always, as was already indicated. Amphoric resonance is an 
indication that the excavation is at least five centimeters in diameter, 
that its walls are smooth, round, and rigid, due to surrounding infil- 
tration or fibrosis; that in all probability it communicates with a 
bronchus of not very wide caliber; and that it is not active—a fibrous 
capsule prevents the absorption of toxic matter from the cavity, and 
also the extension of the lesion, and the small amount of secretion is 
soon eliminated by expectoration. It is for these reasons that cavities 
with amphoric breathing are usually not accompanied by any adven- 
titious sounds, excepting at times by a metallic tinkle, and this is 
very rare; while cavernous breathing is almost always accompanied 
by large or medium-sized consonating rales or gurgles. In the latter 
case the cavity is active, probably growing, and not surrounded by a 
fibrous shell. The prognostic significance is clear. The intensity of 
the amphoric phenomena depends on the stiffness of the wall which, 
in its turn, depends on a strong fibrous capsule, or an infiltration and 
caseation of the surrounding lung tissue. In the former case it will 
not enlarge and may even shrink, while in the latter case the excava- 
tion may extend and usually does. 


408 CHRONIC PHTHISIS, ADVANCED STAGE 


Metamorphosed Breathing.—Over the sites of cavities, mainly over 
the upper lobes, we sometimes hear the inspiratory murmur begin as 
a harsh or bronchial murmur, but during its course suddenly softens 
and changes in tone, finally ending with an amphoric sound. At times, 
both inspiration and expiration are thus affected. Laennec spoke 
of it long ago as a soufle voilé, beginning as vesicular and ending as 
bronchial or amphoric. It seems that it is due to the breathing of a 
cavity. The air enters into a relaxed excavation and the murmur is 
modified, while its walls are being distended or inflated. According 
to Plesch it occurs only when there are slight pleural adhesions over the 
cavity, and when there are small islands of airless tissue or cavities 
scattered in an air containing, but relaxed parenchyma. On the other 
hand, Riess! found that it is audible over cavities into which two to 
four bronchi enter. During inspiration at first one bronchus is open 
while the others happen to be plugged; but soon another one or more of 
the entering bronchi open and introduce another type of sounds. 
It is one of the best signs of an excavation, but it is only rarely met with. 

The India-rubber Ball Sound.—A very reliable sign of a cavity is the 
post-tussive suction sound heard immediately after an explosive cough. 
The patient is made to cough vigorously once or twice while the chest 
is auscultated over the site of We excavation. A hissing sound, as if 
another inspiration had taken place immediately after the patient 
ceases coughing, is heard. At times this post-tussive suction is felt 
with the palpating hand laid over the chest wall. It appears that this 
phenomenon is heard only in patients with cavities with yielding walls, 
which become more or less compressed during cough, and reéxpand 
immediately after the cough, sucking in air, thus producing a hissing 
sound plainly audible through the stethoscope. It is this sound that 
suggested the analogy with the india-rubber ball. It is usually heard 
over pulmonary cavities, but Bergmark reports that it may also be 
heard over pleural adhesions. 

Adventitious Sounds Heard over Cavities.—Over excavations, large 
moist, bubbling, consonating rales—called in text-books metallic or 

cavernous rales—are often heard. They are caused by the air stream 
passing through the collection of fluid in the excavation. ‘The size, 
pitch, timber, and duration of these rales depend on the size of the 
vomice in which they originate, as well as the condition of its walls— 
whether they are smooth or ragged, rigid or relaxed, ete. On the 
other hand, over old cavities there may be audible amphoric breathing 
of an exquisite type, metallic breathing without any rales at all, 
because the fibrous walls do not secrete any more. ‘These are cases 
that are doing well for years in spite of extensive excavations. In 
many arrested cavities there remain creaky sounds, especially when the 
plural sheets are not at all adherent, or when the adhesions are but 
partial, so that there are differences in the elasticity of various parts 
of the affected area of the lung. 


1 Deutsch. med. Wehnschr., 1917, 43, 392. 


BASAL CAVITIES 409 


In many cases the number of rales in excavations and their intensity 
are so great that they obscure all the breath sounds. 

The metallic tinkle is only rarely heard over pulmonary cavities. 

Pectoriloquy is met with over pulmonary cavities, but it is not 
pathognomonic of this condition. In many cases we hear the voice 
as if it is directly spoken into the ear with abnormal clearness. It 
merely indicates that the conditions for conduction are unusually 
good, which may be true of excavations, but are also met with in 
pneumothorax, and even in consolidated lung tissue through which a 
bronchus passes. 

The same is true of whispered pectoriloquy. But the transmission 
of the whispered voice with a metallic or amphoric echo, which Kuthy 
calls “amphorophony,” is a sure indication of a smooth-walled cavity 
filled with air, either pulmonary or pleural, 7. e., a tuberculous excava- 
tion or a localized pneumothorax. The differential diagnosis between 
these two conditions can, at times, be made out by the x-rays, but I 
have met with cases in which roentgenography was not decisive. Some 
cavities can be made out by auscultation with much less trouble 
and greater reliability than by other diagnostic methods. Ampho- 
rophony is, however, only audible over old and larger cavities which are 
stationary, while over acutely progressive and extending vomicee it is 
only rarely heard. In many cases of localized pneumothorax I have 
found distinct whispered pectoriloquy in the axilla, which is exceedingly 
rare in cavity. This is a sign of great value in attempts at differentia- 
tion between these two conditions. 

Basal Cavities.—The vast majority of tuberculous cavities are formed 
in the upper lobes of the lungs, except in the terminal stages, when 
the resistance is very low, excavations then extending into the lower 
lobes of the lungs. 

They are very difficult of diagnosis. We may find signs of excava- 
tions at the base which are really “phantom caverns,” as William 
Ewart! called them. The amphoric sounds of an excavation in the 
upper lobe are transmitted to the base by some transient or permanent 
consolidation. Echo may also be responsible for cavernous sounds 
at the base when the original excavation is situated in the opposite 
side of the chest and not in immediate contact with the spinal column. 

Basal cavities were rare in phthisical persons, but of late more of 
them are encountered. It seems that in many cases, even when 
occurring in tuberculous patients, they are of influenzal origin. Many 
tuberculous patients who were attacked by epidemic influenza and 
bronchopneumonia remained with interstitial pneumonic lesions in 
the lower lobes of the lung, especially the left lung. In these patients 
the tuberculous process in the upper lobe pursues its course almost 
unaffected by the bronchiectatic lesion in the lower lobe; but they 
cough and expectorate much more severely than those who are free 


1 Goulstonian Lectures, British Med. Jour., 1882. 


410 CHRONIC PHTHISIS, ADVANCED STAGE 


from this complication. The number of this sort of cases has very 
much increased during recent years. 

It is important to mention that the prognosis is more unfavorable 
in tuberculous basal cavities than in those located in the upper lobes, 
undoubtedly because they do not empty themselves with ease. Con- 
sidering a pulmonary cavity as an abscess, we understand that when it 
does not drain the result must be disastrous; the abundant secretions 
fill it up, and cough is not very effective in removing them. In the 
terminal stages of phthisis with lesions in the upper lobe, excavations 
sometimes form at the base, as we find them at necropsy, and kill the 
patient who may have been getting along very well before their 
occurrence. In fact, if in the course of chronic phthisis signs of excava- 
tion appear in the lower half of the chest, the prognosis is very gloomy. 

Visceral Displacements.—The displacements of the mediastinal 
organs have already been referred to (p. 401). The heart is in most 
cases of advanced phthisis displaced toward the affected side of the 
chest, and in right-sided lesions we at times meet with complete 
dextrocardia. But in many cases there are also to be noted displace- 
ments of the trachea and larynx, first described by E. Ruedinger.' 
Gerald B. Webb, A.M. Forster, and B. G. Gilbert? described in detail 
the tracheal position in phthisis and suggested an easy method of 
detecting it: By placing the hand behind the neck while the thumb 
anteriorly reaches out to the trachea and rolls it, we can in most cases 
determine its position. It appears that in most cases of early phthisis 
the trachea is displaced toward the affected side. Webb found in 100 
cases of pulmonary tuberculosis of all ages the recognition of the 
side especially affected proved correct in 69, doubtful in 19, and 
incorrect in 12 cases. It is due to pleural adhesions, together with 
fibrosis in the lung or pulmonary retraction pulling the trachea along. 

This deviated trachea is occasionally a source of error in diagnosis. 
When it is displaced to the margin of the sternum, we hear loud tracheal 
or even “cavernous” breath sounds both anteriorly and posteriorly, 
and thus diagnose a cavity which does not exist. Especially is this 
error of great moment when the trachea is displaced to the opposite 
unaffected side after the induction of a pneumothorax, and we may 
think that there is a cavity in the untreated lung. Eut a little care 
will usually clear up the case, especially when the possibility of dis- 
placement of the trachea is borne in mind. Webb says that movement 
of the trachea to the side of the healthier lung following the application 
of pneumothorax foretells a successful application of this procedure. 
In my experience this is not invariably the case. 

In many cases there is also upward displacement of the stomach 
and liver after pulmonary retraction. 

Duration of the Disease.—The duration of chronic phthisis is vari- 
able. Some patients get well, or succumb, within one year, while in 


1 Beitr. z. Klin. d. Tuberkulose, 1910, 17, 151. 
2 Jour. Am. Med. Assn., 1915, 65, 1017. 


DURATION OF THE DISEASE 411 


most the sluggish course continues intermittently for many years, 
during which period the patients consider themselves cured, and 
suffer from “relapses” several times. They constitute the bulk of 
the class of patients who are admitted to sanatoriums and hospitals 
for consumptives several times. The reason is clear when we bear in 
mind the oscillating course of the disease—during acute or subacute 
exacerbations they seek relief in institutions, while during remis- 
sions, when the process is quiescent, they believe that they have been 
cured, or the disease has been arrested. 

Basing their estimates on heterogeneous material, different authors 
have estimated the average life of the consumptive as at from one to 
ten years. Leudet! found that of hospital patients 90.7 per cent die 
within five years of the onset of the first symptoms; 9.3 per cent 
during the sixth to the nineteenth year. He also found that among 
the more prosperous patients only 77.2 per cent die within the first 
five years, and 22.8 per cent between the sixth and the nineteenth 
years. Brown and Pope,’ studying statistically the outlook of patients 
discharged from the Adirondack Cottage Sanitarium, found that of 
those discharged “apparently cured” at the end of five years, 94 per 
cent of the expected were alive; at the end of ten years, 86 per cent. 
In those “arrested” the proportions for the corresponding years were 
63, 49 and 46 per cent; and for those “active,” 25, 15 and 10 per cent. 
It is thus clear that “an arrested’”’ or even an “active” case is not 
necessarily doomed. There are always good chances to live for long 
years. 

The striking disparity in these two sets of statistics is due to the 
difference in the material. Leudet studied only fatal hospital cases, 
without including any of those who survived twenty years, while 
Brown and Pope studied cases discharged from a good sanatorium in 
which moderately well-to-do patients predominate, and among whom 
a fairly large proportion were affected with the abortive type of the 
disease. 

Attempts at estimating the average duration of life of the consump- 
tive have also met with failure because it is difficult to obtain com- 
parable material. When only acute, progressive cases are considered, 
the average is a low figure, one year or even less; when abortive cases 
are considered—and they are mostly those which have been diagnosed 
exceedingly early in the disease—the average is very high. It is for 
this reason that the “averages” vary from one to ten years, according 
to different authors. 

But for the individual patient, with whom the physician deals, 
averages do not count for much. He must be judged by the clinical 
manifestations. It may be stated that those who have long periods 
of quiescence live long; many practically their natural lives. ‘They 


1 Quoted from Kuthy and Wolff-Eisner, Prognosenstellung d. Tuberkulose, Berlin, 
1914, p. 56. 
2 Am. Med., 1904, 8, 879; Ztschr. f. Tuberkulose, 1908, 12, 205. 


412 CHRONIC PHTHISIS, ADVANCED STAGE 


may be “cured” several times when they suffer from acute or subacute 
exacerbations, but they recuperate every time and live on, often 
with quite some efficiency. On the other hand, in the case of those in 
whom acute or subacute exacerbations are frequent, and each is of 
long duration, a fatal issue is inevitable sooner or later. 

Modes of Death.—Death supervening during an acute exacerba- 
tion, when the process in the lungs is extending, or the toxemia is 
severe, or the resistance is low, may be rapid, like from pneumonia 
or septicemia. The patient may have done quite well, but is suddenly 
stricken with high fever and prostration, and he succumbs to dyspnea, 
cardiac failure, etc. At the autopsy acute miliary tuberculosis is 
found in these cases. Usually the process is slower; the high con- 
tinuous or remittent fever, the profuse nightsweats, anorexia, dysphagia 
due to laryngeal ulceration, extreme emaciation, etc., keep on for weeks 
or months; the patient is gradually but surely consumed by the dis- 
ease. In some, the last few weeks resemble in their symptomatology 
the typhoid state with marked prostration, muttering delirium, etc., 
which, again, is an indication of complicating miliary tuberculosis. 

In others, the cachexia progresses despite the fact that the fever is 
low, hardly ever exceeding 101° F., and the patients finally die from 
asthenia, like those suffering from malignant disease. Excepting the 
cough, diarrhea, and weakness they do not suffer much and, because 
the sensorium is well retained to the end, the euphoria may be exquisite. 
Others consider themselves quite well despite the extreme emaciation 
and attempt to walk around, against the advice of their physician, and 
among them death due to asystole the result of toxic myocarditis— 
the poisoned heart of Sir James Mackenzie, may occur. Some of these 
unfortunates are occasionally found dead in bed in the morning. But 
in such cases it may not have been syncope, but a heavy dose of some 
opiate which abolished the reflexes, prevented cough and expectoration, 
and they were drowned by their own secretions. Other causes of 
sudden death during the night are sudden onset of pneumothorax, 
copious hemorrhage, etc., killing before aid can be summoned. 

Complications of the disease are often responsible for a fatal issue. 
Among the most important are pulmonary hemorrhage and pneumo- 
thorax. While 98 per cent of patients who suffer from more or less 
bleeding survive the accident, 2 per cent succumb to it. The patient 
may feel comparatively well, and in fact consider himself on the way 
of recovery, or even cured, when suddenly brisk and profuse hemor- 
rhage occurs and kills him. Emaciated patients may die as a result of 
suffocation with their own blood, being powerless to expel it from the 
chest. 

Pneumothorax is the cause of death in about one of 150 fatal cases 
of phthisis. This may kill the patient within one or two days, the 
cause of death being asphyxia, or within a few weeks or months through 
complicating pyothorax. 

Complicating laryngeal tuberculosis is responsible for the death of 
many patients through dysphagia, dyspnea, edema of the glottis, ete. 


PREMONITORY SIGNS OF DEATH 415 


Between 5 and 10 per cent of deaths from phthisis are preceded by 
cerebral symptoms. Most of these are due to tuberculous meningitis, 
but some are also caused by uremia, as was already stated. 

Premonitory Signs of Death.—In chronic phthisis with tendencies 
to a fatal issue, it is often very difficult to prognosticate the time 
when the end will come. Indeed, the more extensive the experience 
of a physician with this disease, the more guarded he becomes in 
foretelling the day of death. Such statements as “he cannot survive 
three days,” or “he will surely die within a week,” etc., should be 
avoided. Some patients keep on living for weeks or months under 
conditions which are puzzling, to say the least. 

There are symptoms and signs which may, however, be considered 
precursors of death in phthisis. Of these we may mention: Dvys- 
phagia, due to laryngeal ulceration, when not quickly relieved by 
treatment, is a sure indication that the patient will not survive very 
long. The same is true of profuse diarrhea which cannot be controlled 
by treatment. ‘lhe emaciation is extreme, and the end comes rapidly. 
But I have seen cases with profuse diarrhea lasting for months, in spite 
of the fact that they hardly assimilated any nourishment. The reason 
is clear when we consider that the emaciated victim of phthisis lies 
quietly, hardly moving a limb, or expending any energy, so that the 
least fuel is sufficient to keep the spark of life aglow. 

Edema of the extremities very often appears shortly before death. 
It is usually due to cardiac weakness or nephritis, thrombosis or 
thrombophlebitis. It may be unilateral, but usually both lower 
extremities are affected. The swelling may be enormous in extreme 
cases, while in most it is but moderate and tender on pressure. When 
this edema of the lower extremities is combined with cyanosis and 
dyspnea, a fatal issue may be expected within a month. Thrombosis 
of the femoral, jugular, subclavian, or other veins is one of the surest 
premonitory signs of death. A sudden elevation of the temperature, 
accompanied by severe dyspnea, cyanosis, the typhoid state, muttering 
delirium, etc., is an indication of complicating acute miliary tuber- 
culosis from which recovery is not to be expected. 

Aphthous stomatitis commonly portends death. In some cases 
treatment may improve the condition in the mouth, but within a few 
weeks the powers of life wane and death supervenes. Another sign 
which justifies information to relatives that the end is near is a red, 
spongy condition of the free edge of the gums. 


CHAPTER XXL 
ABORTIVE TUBERCULOSIS. 


Natural Resistance Against Phthisis.— As was already shown, infec- 
tion with tubercle bacilli is harmless to the vast majority of civilized 
people; the lesion cicatrizes more or less quickly without producing 
distinct clinical symptoms. During childhood, when most infections 
occur, the morbidity and mortality from this disease are insignificant. 

We cannot recognize these mild or abortive infections clinically, 
except by the tuberculin test; they probably pass as slight or severe 
“colds,” grippe, bronchitis, ete. Nor do we know whether they are 
due to the inoculation by strains of bacilli of low virulence, considering 
the marked difference in virulence displayed by various strains of 
tubercle bacilli. The suggestion that they may be due to infection 
with bovine bacilli appears to have much in its favor, but this also 
has not been proved. 

Clinical evidence seems to point in another direction as to why some 
tuberculous lesions are abortive. As will be shown later on (see p. 607) 
individuals with normal or excessive action of the thyroid gland only 
rarely suffer from acute and progressive phthisis; likewise those in 
whom the lymphoid apparatus is hypertrophied, especially of the 
“lymphatic diathesis,’ only rarely succumb to tuberculous disease. 
It is in fact rare to meet phthisical patients with enlarged lymphoid 
tissues in the throat. When tuberculous lesions are discovered in 
these individuals, they are either quiescent, or altogether sclerosed, and 
have hardly any symptoms. In his study of such lesions, Eugene L. 
Opie! found that healed and in great part calcified lesions in persons 
who died from non-tuberculous disease are almost invariably accom- 
panied by hypertrophy of the lymphatic glands in which tuberculous 
lesions tend to heal even when extensive. In other words, individuals 
with properly active lymphoid glands are likely to suffer from abortive 
tuberculosis when infected with tubercle bacilli. This subject deserves 
further investigation. 

We meet at times cases of abortive tuberculosis, 2. ¢., patients in 
whom the disease, instead of pursuing the usual clinical course to its 
termination in death or recovery after several months’ or years’ illness, 
as aborted within a few weeks or months of indisposition. In other words, 
just as we at times meet with cases of abortive pneumonia, typhoid, 
scarlet fever, etc., so is there a form of pulmonary tuberculosis which 
is of relatively short duration and invariably terminates in recovery. 


1 Am. Rev. Tubercul., 1920, 4, 629. 


SYMPTOMATOLOGY OF ABORTIVE TUBERCULOSIS 415 


In these cases the lesion is apparently circumscribed, of little activity, 
often altogether latent and quickly cicatrizes, and, when the patient 
dies from any other cause, it is found at the autopsy in the shape of 
more or less extensive scars located at the extreme apex, pleural 
adhesions, or even isolated fibrous or calcareous nodules which hardly 
caused any inconvenience to their owners during life. 

In the older works on phthisis, this form of tuberculosis is not men- 
tioned at all. In former days only advanced phthisis was recognized. 
But in recent years, since Bard! described the pathology and symptom- 
atology of tubereulose abortive, many others have mentioned it more 
or less extensively. In the second edition of Cornet’s? treatise, also 
in Bandelier and Répke’s book, we find it mentioned cursorily, while 
Piéry® in his book devotes an extensive chapter to it. Bezancon‘ and 
the present author® have published papers on the subject of abortive 
tuberculosis. 

Abortive tuberculosis is responsible for a large proportion of “non- 
tuberculous” cases in sanatoriums—the lesion heals very quickly and 
it is often suspected that the patients were admitted through an 
error in diagnosis. Many of the patients who state that well-known 
physicians have considered them tuberculous at one time, but that they 
have none the less been healthy all along for years, have in fact been 
affected with the abortive type of the disease at the time the diagnosis 
was made. I have seen many patients who applied for admission to 
public sanatoriums and were passed by the admitting physicians as 
eligible incipient cases, but inasmuch as the institutions were over- 
crowded, they had to wait for weeks or months for vacant beds. When 
they were finally called, it was found that all the symptoms and signs 
of the disease had vanished. As will be shown later on (see p. 486), 
many of these cases are instances of apical tuberculous pleurisy. The 
prognosis in tuberculous pleurisy is usually better than in paren- 
chymatous lesions. A large proportion of cases of “persistent colds,” 
grippe, rhinopharyngitis, etc., are also abortive tuberculosis. If 
they were carefully studied, we would discover some physical signs in 
the chest substantiating this view. In fact, L. Napoleon Boston® 
reports finding tubercle bacilli in cases of acute colds, influenza, 
bronchitis, etc., but the patients recovered without becoming tuber- 
culous. Many of these were in fact abortive tuberculosis. 

Symptomatology of Abortive Tuberculosis.—Vhe symptoms and 
signs of abortive tuberculosis are the same as those of incipient phthisis, 
but they never pass beyond that stage. In most cases it begins with 
the symptoms of a common “cold.” After some exposure the patient 
begins to cough, has some fever, malaise, backache, etc., and is treated 
Formes cliniques de la tuberculose pulmonaire, Genéve, 1901. 

Die Tuberkulose, Vienna, 1907, p. 690. 
La tuberculose pulmonaire, Paris, 1910, p. 491. 
Bull. Soc. hép. de Paris, 1901, p. 933. 


Medical Record, 1913, 82, 921. 
Interstate Med. Jour., 1914, 21, 330. 


on pgp. Oo Ne 


416 ABORTIVE TUBERCULOSIS 


for coryza, grippe, tonsillitis, ete. But instead of ameliorating within a 
few days or a week, the symptoms persist for a month or two. In 
many cases the onset is marked by hemoptysis. The patient, who has 
felt quite well, or at most has coughed for a few days, suddenly feels 
some irritation in the throat and coughs out some blood or blood- 
streaked sputum. ‘The bleeding may last for a few hours or days and 
either stops abruptly, or continues for a few days in the form of streaky 
sputum. Many tuberculous patients give histories of one or more 
attacks of abortive tuberculosis years before the onset of symptoms of 
active phthisis. The last attack is not “aborted.” Every physician 
has among his clientele patients who expectorated blood years ago, 
but have felt well all along. While in many of these the hemor- 
rhage was of extrapulmonary origin, as was already shown, in others it 
was due to abortive tuberculosis. 

When the thermometer is carefully and judiciously used, we find 
fever of a mild type; especially in the afternoon there is a rise of one 
or two degrees, and in the early morning there may be some subnor- 
mal temperature. In some cases that came under my observation I 
found the typical temperature curve of mild incipient phthisis, and 
there were many of the accompanying symptoms of hyperthermia— 
malaise, languor, pain in limbs, backache, etc. While the patient is 
not completely incapacitated, yet he feels tired during the afternoon, 
but recuperates in the ev ening, or feels refreshed after a night’s sleep. 
Nightsweats are rare, but in a few I have noted that they were drench- 
ing. ‘The appetite is usually retained and when the patient is told 
to eat well and plenty, he finds no difficulty in following instructions. 

Cough is a constant symptom; though many state that they do 
not cough, careful inquiry reveals that they clear their throats in the 
morning. We often meet with dry, hacking cough which is an annoy- 
ance during the day, and keeps the patient awake during the night. 
Occasionally the cough is productive of glairy mucus, but the muco- 
purulent sputum of vane ice is never seen in abortive cases, unless 
there is some rhinopharyngitis. 

Most akortive cases are of the “closed”’ variety of tuberculosis, but 
now and then we meet with one showing tubercle bacilli in the sputum. 
Considering that a considerable proportion of these cases have hardly 
any parenchymatous lesion, but are in fact instances of apical pleurisy, 
it is clear that tubercle bacilli in the sputum should be detected only 
exceptionally. 

In some, we meet with hoarseness lasting intermittently for a few 
hours during the day, or for several days in succession. 

Tachycardia is not a very frequent symptom, but we very often find 
instability of the pulse; the least exertion or excitement raises its 
rate to 90 or more per minute. The blood-pressure is usually lower 
than normal. With the improvement in the condition of the patient 
both the pulse and the blood-pressure become normal again. 


DIAGNOSIS 417 


Physical Signs.—The objective signs are those of incipient phthisis. 
Of course, when the lesion is limited and centrally located, we may 
not find any physical signs at all, and without hemoptysis and tubercle 
bacilli in the sputum, the diagnosis cannot be made. In all proba- 
bility the vast majority of tuberculous infections in man are of this 
character. They are aborted without revealing themselves in any 
way. But in those in whom the conglomeration of tubercles is large 
enough to alter the air content in a limited area of the lung, we may 
find signs on percussion and auscultation. 

A short note above and immediately beneath the clavicle is quite 
common. But this may be obscured by vicarious emphysema, hyper- 
function, or relaxation, of the surrounding lung tissue which may emit 
a hyperresonant note. Shortening of an apex, or narrowing of Kronig’s 
resonant areas, is more common and can be easily made out with careful 
percussion. 

On auscultation we may hear feeble breath sounds over the site 
of the lesion, or rough, interrupted, cog-wheel breathing. Only the 
inspiratory murmur is usually altered, but I have seen cases in which 
the expiratory murmur was prolonged, and even bronchovesicular 
in character, indicating extensive infiltration, yet recovery went on 
speedily, showing that even a considerable focus may be aborted. 
This is confirmed by the large scars or encapsulated and calcified 
tubercles found at times while making autopsies on persons who died 
from causes other than tuberculosis. 

Adventitious sounds are not often heard, excepting in those who 
have had hemoptysis and in some grippal cases, in which dry crackles, 
of crepitation, may be audible during inspiration and influenced by 
cough. In many a friction sound is audible over the supraspinous 
fossa, in the “alarm zone.” There are instances of apical tuberculous 
pleurisy which is described elsewhere (see p. 486). Of course, to be of 
significance, these signs must be strictly localized at one apex, and 
constant for some time. They must also be differentiated from 
spurious rales, as well as from marginal sounds. 

Roentgenography is of little value, as was already stated in Chapters 
XVII and XIX. 

Diagnosis.—These are the classical symptoms and signs of incipient 
phthisis, and when meeting with a case we are by no means certain 
as to the course the disease is likely to take. In fact, many abortive 
cases are admitted to sanatoriums where they are speedily cured, 
and they contribute no small portion of the statistical success of 
institutional treatment. 

In the progressive cases the lesion extends and the constitutional 
symptoms become more and more marked within a few months, while 
in the abortive form the mild fever, cough, nightsweats, etc., abate 
within a few weeks or one or two months, and the physical signs dis- 
appear, or they are superseded by sibilation, and there may perma- 
nently remain a prolonged expiratory murmur over the affected apex. 

27 


418 ABORTIVE TUBERCULOSIS 


While in most cases the local impairment of resonance remains, and for 
this reason there are many persons in whom there are differences in 
this regard when the two apices are compared, I have observed that in 
some even this disappears, to be replaced by slight hyperresonance, 
due probably to hyperfunction, the result of vicarious emphysema of 
lung tissue around the cicatrix which was caused by the healing 
process. 

Without observing the patient for several weeks, and without an 
initial pulmonary hemorrhage, or tubercle bacilli in the sputum, 
abortive tuberculosis cannot be diagnosticated, because there always 
lurks a suspicion that it may have been a non-tuberculous apical lesion. 
There are, however, some points which may help us in recognizing 
this form of tuberculosis: When a patient with a distinct apical lesion 
has a good appetite and normal gastric function, gaining weight and 
strength as soon as he begins to take care of himself, there is a likeli- 
hood that the lesion may be aborted and cured within two or three 
months. However, this may prove deceptive at times. Some points 
which have helped me are the following: A slow pulse, not much 
influenced by exertion or excitement, speaks for a benign process. 
The initial hemopty sis of chronic phthisis, as was already stated, is 
usually preceded by cough, weakness, nightsweats, ete., for weeks 
before the bleeding, while in abortive cases this is rare =the hemoptysis 
comes like a thunderbolt out of a clear sky, without any premonitory 
symptoms and without any apparent exciting cause. In progressive 
cases the initial hemoptysis is usually more eben lani and always fol- 
lowed by fever of the type described above. In abortive tuberculosis 
the temperature remains normal at times, but usually it is slightly 
elevated, 1° or 1.5° F. for a couple of weeks. Initial hemoptysis of 
tuberculous origin without high or moderate fever, and without tachy- 
cardia, weakness, languor, etc., points to an abortive lesion. 

In the majority of cases, however, only careful observation of the 
course of the affection is decisive. Moreover, abortive tuberculosis is 
apt torecur. As was already stated, in many cases the exacerbations 
abate, but now and then the new attack persists and then symptoms 
of chronic phthisis make their appearance. At times the subsequent 
attack manifests itself by acute and progressive course, again confirm- 
ing the observations that acute tuberculosis lesions in adults are 
antedated by milder attacks. 


Lig 7a af bali a) >, AE 
FIBROID PHTHISIS. 


Fibrous Hyperplasia in Phthisis.— Discussing the morbid anatomy 
of phthisis, we showed that while the tuberculous process is mainly 
one of destruction—infiltration, caseation and softening—there are 
reparative forces at work in almost every case, manifesting themselves 
principally in the formation of connective tissue which either heals 
the lesion through cicatrization, or at least limits its progress. In fact, 
it may be said that without the formation of connective tissue, every 
case of phthisis would be acute. The balance between the destructive 
and reparative processes in phthisis depends consequently on the 
amount of fibrosis within and about the lesion—the more intense the 
formation of fibrous tissue the slower the progress of the disease, and, 
conversely, the more caseation and necrosis, the more acute and pro- 
gressive the disease. 

We must distinguish between fibrosis and formation of cicatrices. 
When a lesion cicatrizes, the activity of the tuberculous focus is 
extinguished, though without any restitutio ad integrum, as is seen in 
healed tuberculous lesions of the lungs and pleura. But in fibrosis 
the lesion is an active, inflammatory process, though it may be only 
slightly progressive, yet connective tissue is being continually produced. 
In other words, in fibroid phthisis the destructive process is smoulder- 
ing, though in abeyance, or entirely absent, and the proliferative pro- 
cess dominates. As Bard says, the lesions may be progressive and 
spreading, though they are not of a destructive character. 

It must also not be confused with fibroid degeneration of the pul- 
monary parenchyma which at times follows acute or chronic non- 
tuberculous inflammatory processes of the lungs, such as the so-called 
interstitial pneumonia, pulmonary induration, or cirrhosis, ete. 
Fibroid phthisis is a specific proliferation of the lung tissue caused by 
tubercle bacilli. 

Clinically this form of tuberculosis is characterized by an exceedingly 
chronic course extending over many years, finally leading, in most 
cases, to the development of the symptoms and course of the common 
form of chronic phthisis. It differs from other forms of inflammatory 
fibrous degenerations of the lung in that it is caused by tubercle 
bacilli, and that characteristic tuberculous giant cells are found 
microscopically in the lesions of fibroid phthisis. 

Fibroid phthisis was mentioned by Bayle one hundred years ago 
and ever since by many others; Sir Andrew Clark! coined the term, 


1 Fibroid Diseases of the Lung, London, 1906. 


420 FIBROID PHTHISIS 


and made a thorough study of the pathology and symptomatology of 
the disease. C.J. B. and C. T. Williams,’ in their book on consump- 
tion, also give a complete description of this form of phthisis. Of 
the more recent writers who treat of this subject may be mentioned 
Bard,? Sokolowski,? and Piéry.4. While most of the authors do not 
agree on the various points which characterize fibroid phthisis, yet in 
the main they are in agreement on its differentiation from all other 
forms of pulmonary tuberculous disease. 

Etiology. — Fibroid phthisis is mainly encountered in persons between 
forty and sixty years of age and, contrary to the statements of many 
authors, it may occur in younger individuals. Apparently many cases 
are treated for chronic bronchitis, asthma, pulmonary emphysema, 
etc., and only after the process has lastéd for many years is the char- 
acter of the affection recognized; an intercurrent hemorrhage, or 
tubercle bacilli in the sputum, reveals the true nature of the disease. 
I have met with many cases in persons under thirty years of age. 

It appears that syphilis is an important etiological factor; when 
both tuberculosis and syphilis are met with in the same individual, the 
process of the former is often of the fibroid type. Sergent’ and several 
other French writers have indeed maintained that most fibroid cases 
are a manifestation of syphilis and tuberculosis. Several English 
authors hold the same view. Thus, J. Mitchell Bruce® says: “It 
should be noted that some cases of quiescent phthisis give a history 
of syphilis which may account for the disposition to fibrosis, and 
pro tanto may be a favorable element prognostically.”’ In my expe- 
rience this holds true for some cases, but not for the majority. I have 
seen many cases of fibroid phthisis in which specific disease was posi- 
tively excluded, and at the Montefiore Hospital, where we have many 
of these cases, the Wassermann reaction is only rarely positive, and 
the other stigmata of syphilis are lacking in the majority of cases of 
fibroid phthisis. 

English authors, notably Clark, have observed that the gouty 
diathesis, which is antagonistic to tuberculosis, is responsible for the 
fibroid form of phthisis. This is not in agreement with my experience, 
because among the poor in New York City gout is rather rare, while 
fibroid phthisis is quite common. Nor have I found any etiological 
relations between fibroid phthisis and alcoholism, or social and eco- 
nomic conditions, ete. 

It appears to me that occupation is of greater etiological moment. 
Most of the cases I have seen were in persons working indoors, inhal- 
ing animal and vegetable dust—garment-workers, furriers, rag-pickers, 


1 Pulmonary Consumption, London, 1887. 

2 Forms cliniques de la tuberculose pulmonaire, classification et description sommaire, 
Genéve, 1901. 

8’ Klinik der Brustkrankheiten, Berlin, 1906, 2, 410. 

4 La Tuberculose pulmonaire, Paris, 1910. 

5 Presse médicale, 1908, 16, 657. 6 Lancet, 1913, 1, 591. 


FORMS OF FIBROID PHTHISIS 421 


ete. It seems also that chronic lead poisoning is a predisposing factor, 
because of its frequency among plumbers, printers, and house painters. 
In former days it was frequently seen among chimney-sweepers, and 
today it is met with among those who inhale any irritative dust, as 
knife-grinders, coal-heavers, button-makers, ete. 

Pathology.—The pathology of fibroid phthisis has been thoroughly 
studied by Sir Andrew Clark, who described that the affected lung is 
usually decreased in size; sometimes its dimensions do not exceed the 
size of a closed fist. In local fibrosis only the affected part of the lung 
may be contracted, while the rest fills up its place by compensatory 
emphysema. Cavities—pulmonary and bronchiectatic—are common, 
surrounded by dense, rigid walls. Cheesy nodules encapsulated by 
fibroid tissue are frequent, and during the final stages the caseating 
process gains the upper hand and breaks through the limiting and 
protective fibrous tissue spreading the destructive process. ‘The 
walls of the alveoli are thickened and finally obliterated or filled in, 
the interlobar connective tissue, especially around the large vessels and 
bronchi, proliferates enormously and, replacing the parenchymatous 
tissue of the lung, produces a state of induration through which the 
dilated bronchi pass. 

In all cases of fibroid phthisis the pleura is thickened over the 
affected area, sometimes attaining a thickness of one-half to three- 
fourths of an inch. The pleural cavity is adherent and, in the pleural 
form, obliterated by tough fibrous tissue binding the two surfaces 
together, and from it other bands of connective tissue are sent forth 
into the lung which contract and drag along toward the affected side 
the mediastinum, the diaphragm, and with it the liver, etc. 

We are not clear why the tubercle bacilli produce caseation and 
liquefaction of tissue in most cases, while in others a proliferation of 
connective tissue is the dominant feature after infection. We know 
that in many cases of fibroid phthisis we have an additional etiological 
factor, the inhalation of mineral, animal, and vegetable dust. But 
on the other hand, the form which will be described as the pleural 
form of fibroid phthisis is not usually associated with the inhalation 
of irritating dust, but the causative factor seems to be bacterial, plus 
the predisposing factors which are operative in the other forms of 
chronic phthisis. 

We are in the dark about these problems. It has not been proven 
that in fibroid phthisis the tubercle bacilli are of some attenuated 
strain, or of the bovine type. In many cases of fibroid phthisis in which 
tubercle bacilli are not detected, Much’s granules have been found, 
thus pointing to bacilli which have lost their acid-fast properties 
being the cause; but this also requires further study. 

Forms of Fibroid Phthisis.—The symptomatology of fibroid phthisis 
depends on the form of the disease. My experience is in agreement 
with that of Sokolowski, excepting that I meet with a pleural form in 
addition to his two forms—simple fibroid phthisis, and fibroid phthisis 


422 FIBROID PHTHISIS 


with emphysema. The most common clinical form encountered by 
me is the emphysematous. 

The Emphysematous Form.—These patients give a history of cough 
dating back many years; some state they had coughed as far back as 
they can recollect. Slight exertion produces dyspnea, and in some 
slight cyanosis of the lips and finger tips may be observed. They state 
that they had consulted physicians repeatedly and were informed that 
the trouble was not of serious import; that it was chronic bronchitis, 
pulmonary emphysema, etc. Inasmuch as they are able to pursue 
their occupations, they more or less disregarded the cough, expectora- 
tion, dyspnea, etc. During the winter and autumn these patients are 
usually subject to “colds,” “ grippe,”’ ete., when the cough is aggravated 
and persists for several weeks with greater severity than usual. 

In some patients, especially those engaged in trades involving the 
inhalation of animal or vegetable dust, the signs of pulmonary emphy- 
sema, as well as attacks simulating bronchial asthma, are apt to come 
on suddenly in one who had never before suffered from any respiratory 
trouble. In fact, experience has taught me to look with grave sus- 
picion on emphysema or asthma coming on suddenly in a person over 
thirty years of age. 

During the early stages of the disease, and this may last for many 
years, the patient, though coughing and suffering from mild dyspnea, 
pursues his vocation without interruption. Fever is lacking, excepting 
during an acute exacerbation, or some intercurrent affection. The 
expectoration is scanty; in fact, the cough is usually dry, or some glairy 
mucus is brought up after a fit of coughing. A search for tubercle 
bacilli is usually fruitless. But the dyspnea is annoying and increases 
on slight exertion. 

The general appearance of the patient is that of a healthy person, 
the panniculus adiposis is well preserved, and in those who do not 
work at hard manual labor, and in women, we may meet with marked 
obesity. The “fat phthisis,”’ of which we speakelsewhere, is seen almost 
exclusively in fibroid patients. On the other hand, there are some 
patients who are more or less emaciated, but they are usually indi- 
viduals who have never been fat; but even they gain rapidly after the 
physician urges them to rest and feed up. I have met with some 
who gained twenty or even more pounds in a couple of months and 
retained it for years. 

The vast majority of fibroid patients have clubbed fingers and curved 
nails. The most exquisite forms of drumstick fingers may be found 
among them, while they are not so common among those who suffer 
from common chronic phthisis. 

Many get along fairly well for years without suspecting the real 
nature of their trouble, until they are suddenly seized by attacks of 
hemoptysis which may be slight, or quite profuse, but which usually 
frighten them out of their wits. In some, the hemoptysis recurs at 
frequent and irregular intervals, and may, at times, be copious, while in 


COURSE OF THE DISEASE 423 


the majority it occurs only rarely and consists only in one or two 
mouthfuls of blood or streaky sputum. It may appear suddenly 
while the patient has considered himself in excellent condition. 
Hemorrhagic phthisis usually is fibroid phthisis, and most patients bear 
the bleeding very well indeed. I have had patients who were so used to 
hemoptysis that it no longer frightened them. We meet with many 
who never expectorated blood. 

Well-to-do patients without profuse hemoptysis get along for years 
without troubling themselves about the cause of their mild cough 
and dyspnea, unless they apply for life insurance, and after they are 
rejected for “lung trouble’’ they promptly consult a physician. It is 
noteworthy that during the early stages of the disease most of these 
individuals easily pass the medical examination for life insurance. 

Physical Signs.—A physical exploration of the chest usually reveals 
an emphysematous, or barrel-shaped, chest in those who suffered for 
years, while in those who have only recently acquired the disease, 
the thorax may be of normal shape. Careful inspection shows some 
flattening of the supraclavicular, infraclavicular, and supraspinous 
fossee, more marked on one side of the chest, wasted muscles of the 
neck and shoulder, and shoulder droop on the same side, coupled with 
lagging and restricted motion. On percussion, defective resonance, 
or even dulness, is elicited on one side above the second or third rib 
anteriorly and posteriorly, while below, and all over the opposite side 
of the chest, the note is hyperresonant, or slightly tympanitic, and the 
inferior margin of the lung is one or two inches lower than normal 
and hardly mobile. Narrowing of Krénig’s resonant area can easily 
be made out; in fact, it appears somewhat accentuated because the 
opposite unaffected apex is larger, owing toemphysema. Auscultation 
shows feeble breathing all over the chest, while over the site of the 
dulness the expiratory murmur is harsh and prolonged, at times show- 
ing a bronchial timbre. Dry crackles, or rales after cough, may be 
audible, in others sibilant or sonorous rales are heard all over one side 
of the chest. During one of the asthmatic attacks, which in some 
patients are quite frequent, so that they are treated for asthma, we 
hear wheezing, sibilant and sonorous rales all over the chest, exqui- 
sitely simulating bronchial asthma. 

Course of the Disease.—These patients get along quite well till 
they pass middle age. Most of them, if they are under medical care 
at all, are considered individuals who are troubled with chronic bron- 
chitis, pulmonary emphysema, asthma, etc. But sometimes between 

- the age of forty and sixty, though exceptionally I have seen it in 
younger individuals, the clinical picture changes. They begin to lose 
weight gradually and persistently, so that sooner or later they present 
the unmistakable appearance of the average consumptive in the 
advanced stages of the disease. The cough becomes more severe 
and productive of globular and nummular sputum containing tubercle 
bacilli, elastic tissue, etc. The cyanosis and the dyspnea become 


424 FIBROID PHTHISIS 


more and more marked, and finally orthopnea sets in with signs and 
symptoms of dilatation of the right heart which is almost constant at 
this stage, followed by edema of the lower extremities, hydrothorax, 
etc. Intestinal and laryngeal tuberculosis are quite common, and con- 
tribute to the misery of the patients who finally expire from asystole, 
or inanition. 

The signs in the chest do not differ markedly from those met with 
in the usual case of far advanced phthisis—signs of cavitation at the 
apices, as well as of diffuse bronchitis are common. Roentgenography, 
which in previous stages showed only signs of emphysema with some 
retraction of one or both apices, now reveals more or less extensive 
cavities and peribronchial infiltration. Displacements of the medi- 
astinum are more frequent than in common chronic phthisis. 

Diagnosis.—In the later stages of the disease the diagnosis is clear 
and it differs from that of chronic phthisis mainly because of the 
dyspnea, cyanosis, edema and clubbed fingers, which are not common 
in the latter condition. In the earlier stages, however, fibroid phthisis 
is difficult to differentiate from pulmonary emphysema, chronic bron- 
chitis and, at times, from bronchial asthma. The persistently negative 
sputum is especially perplexing. Errors may, however, be reduced 
to a minimum by carefully examining the apices in each case of chronic 
bronchitis and pulmonary emphysema. Whenever the physical signs 
point to infiltration of an apex, fibroid phthisis is to be thought of. 
The symptoms and signs of asthma coming on suddenly in one who 
works in surroundings laden with animal, vegetable, or mineral dust, 
usually point to fibroid phthisis. 

Simple Fibrosis.—These are cases of fibroid phthisis in which the 
onset, course, and termination of the disease are practically the same 
as in the form just described, excepting that the symptoms of pul- 
monary emphysema are lacking. The onset is slow and insidious. 
The patient is troubled with an occasional morning cough, expecto- 
rates little or nothing, and the sputum contains no tubercle bacilli or 
elastic tissue. ‘There is, however, slight dyspnea on exertion which is 
often overlooked. 

The general condition of the patient leaves little or nothing to be 
desired. He has no fever, no nightsweats, no anorexia, emaciation, 
etc. All he complains of, if at all, is that he is subject to “colds,” 
especially during the winter months; of breathlessness, and of hemop- 
tysis, which may be quite a feature in this form of phthisis when 
occurring often, or is copious. But before, during, and immediately 
after the hemoptysis there is usually no fever, and convalescence is 
rapid. In fact, many of the patients feel much relieved after the 
effects of a brisk pulmonary hemorrhage have passed away. These are 
the cases which some English authors have described as “arthritic” 
or “gouty” hemoptysis, because some of these patients, though not all, 
present some of the stigmata of the arthritic diathesis. 

Many of these patients present themselves to their physician, who 


DIAGNOSIS 425 


makes a careless examination of the chest and, finding no sign of tuber- 
culous infiltration, assured them that the bleeding came from a ruptured 
bloodvessel in the throat, etc. Thus reassured, they return to work, 
feeling quite well. However, in many there are signs of active phthisis 
in one of the apices: Impaired resonance, contraction of Krénig’s 
resonant area, harsh bronchovesicular, or distinctly bronchial, breath- 
sounds, more or less numerous rales, all localized, circumscribed and 
persistent above the second rib anteriorly and posteriorly over the 
supraspinous fossa in one side of the chest. The physician is often 
amazed to find the patient in such excellent condition for years despite 
the signs of a distinct and active pulmonary lesion, and is apt to 
attribute it to chronic apical catarrh. 

In other cases the onset is, however, not so insidious. A fairly 
healthy person is suddenly seized with a pulmonary hemorrhage which 
may be slight, moderate or, rarely, copious; or he may develop mild 
fever, nightsweats, cough and expectorate sputum containing tubercle 
bacilli. A physical exploration of the chest shows a typical lesion of 
moderate extent. Inasmuch as for several weeks the patient presents 
most of the symptoms and signs of progressive phthisis, even hectic 
fever, nightsweats, emaciation, etc., a grave or doubtful prognosis is 
rendered. 

But slowly the condition of the patient begins to improve; the fever 
abates, the cough is ameliorated or ceases altogether, the appetite 
improves and the patient gains in weight considerably, so that in a 
few months his weight exceeds that found before the onset of the 
disease. He considers himself cured. But a physical examination of 
his chest shows distinct and unmistakable signs of a smouldering 
tuberculous lesion in one apex; in fact, the signs of active disease 
are there and tubercle bacilli may be found in the sputum. Feeling 
well, the patient reénters his occupation and works quite efficiently, 
believing that the physician who declared him still actively tuberculous 
is an alarmist. I have had patients of this class who have been doing 
well for years, and who came around to the office to “ prove’ it to me. 
Many are of the class who were admitted as advanced cases, and then 
discharged from sanatoriums as improved, or even “unimproved,”’ 
and inquiry in later years shows that a large proportion remain in good 
condition and working, except for more or less pronounced dyspnea 
which annoys them. 

After some years the symptoms are gradually aggravated, they 
complain they have “caught a new cold,” which is difficult to cure. 
The cough is persistent and exhausting, the dyspnea distressing, and 
they begin to lose in weight and strength progressively, presenting 
clearly the characteristic clinical picture of chronic phthisis with its 
usual complications, plus dilatation of the right heart, dyspnea and 
orthopnea. Physical exploration of the chest shows the usual clinical 
picture of cavitary phthisis, but there is in addition bronchitis, which 
is unusual in chronic phthisis. It differs, however, from chronic 


426 FIBROID PHTHISIS 


phthisis by the fact that fever is lacking, or, at most, some insignifi- 
cant elevation of temperature is noted at times. No nightsweats are 
present, or only slight, at the end of the disease. 

Pleural Form of Fibroid Phthisis.—In the pleural form of fibroid 
phthisis, the patient usually gives a history of an attack of pleurisy 
with effusion, from which he has recovered after a longer or shorter 
illness, the fluid having been absorbed spontaneously, or was aspirated. 
But ever since he has remained with a dry, hacking cough, productive 
of little or no sputum, and in spite of the great care he has been taking 
of himself, he has not succeeded in recuperating completely. . Dyspnea 
is marked and increasing steadily in intensity. In many cases the 
cyanosis of the fingers and face is very pronounced. 

During recent years I have met with some cases of this type follow- 
ing artificial pneumothorax. A pleural effusion was slow in disappear- 
ing, and the gas inflations had to be discontinued. But the patient 
kept well on the road to recovery, remaining with a pleuropulmonary 
tuberculous lesion. 

Examination shows distinct immobility of the lower half of the side 
of the chest in which the effusion had taken place; some retraction of 
the chest wall and scoliosis, or kyphoscoliosis. Mensuration shows 
that the affected side has fallen in—the circumference being smaller 
than the unaffected side by more than one inch. Vocal fremitus is 
absent over the area. On percussion we find dulness, at times even 
flatness not unlike that over pleural effusion, which is at once sus- 
pected. This is apparently confirmed by the absence of the vocal 
fremitus and of any breath sounds, while in some we hear distant 
tubular, or even cavernous breathing. ‘There may be no adventitious 
sounds, but occasionally some medium-sized or large, moist and con- 
sonating rales and gurgles are audible during both phases of respira- 
tion. At times, distinct friction sounds, grating, and grunts are heard. 
Over the upper half of the chest signs of a tuberculous lesion are usually 
found—bronchial breath sounds, moist rales, and impaired resonance. 
In many signs of a cavity are elicited. 

On the unaffected side signs of pulmonary emphysema are found— 
hyperresonance and the inferior margin of the lung extends two to 
four inches lower than on the opposite side, owing to emphysema, and 
the pulmonary retraction and upward displacement of the diaphragm 
on the affected side accentuate it. Anteriorly, the border of the 
unaffected lung extends well over the sternum. 

The heart is almost invariably dislocated toward the affected. side, 
which serves as a good sign of differentiation from pleural effusion 
with which it may be confused, because in effusions the dislocation 
is invariably toward the unaffected side, if at all. In left-sided lesions 
we may find the apex as far out as the axillary line and one or two 
interspaces higher than the normal; in right-sided lesions the apex 
may be found at the xyphoid cartilage, or even farther to the right. 
It is in these forms of phthisis that acquired dextrocardia is at times 


DIAGNOSIS 427 


found. It is due to traction of the heart by fibrous bands in the right 
pleura and lung and also to the pressure exerted by the vicariously 
emphysematous left lung. The shrinkage, as well as the fibrous bands 
in the lungs, also drag the diaphragm upward and when the right 
side is affected, the liver is also elevated. In the left side the stomach 
may be elevated along with the diaphragm. Pulmonary retraction in 
the left side also exposes the heart and brings it near the chest walls, 
where we may see it pulsating. These conditions may be made out by 
careful percussion, but in many cases the aid of roentgenography is 
necessary to clear up mooted points. 

There are other clinical peculiarities which should be mentioned. 
Fever is usually absent throughout the course, excepting when due 
to some intercurrent affection. When we find a persistent elevation 
of temperature we may look for some complication, especially an 
infiltration of the opposite, hitherto unaffected lung. The cough, 
which was moderate for a long time, in some cases for years, becomes 
more and more severe and the amount of sputum brought up may be 
enormous. Both, the cough and the expectoration, may be influenced 
by posture—the patient coughs more when lying on one side, and is 
somewhat relieved when turning on the other side, just as in bronchiec- 
tasis. This, however, gives no clue as to which side is affected. The 
sputum contains tubercle bacilli in large numbers and is at times fetid, 
which is rare in other forms of phthisis. 

Hemoptysis, which is very frequent in other forms of fibroid phthisis, 
is less often encountered in the pleural form. But when occurring, it 
is apt to last for days or weeks, and at times it is copious. I have seen 
cases in which it was the cause of death of patients who were other- 
wise getting along very well. Most of these patients have clubbed 
fingers and curved nails. 

Dyspnea, which is a feature of all forms of fibroid phthisis, is more 
severe in this type because of the loss of lung tissue and the displace- 
ment of the heart. In fact, I have seen many cases in which the 
lesion in the lung was practically healed, or at least distinctly inactive, 
yet the dyspnea was severe and unbearable. Another feature is 
cardiac palpitation, especially in left-sided lesions, which is apt to be 
so severe as to make life unbearable. 

In the terminal stages signs of cardiac dilatation set in—edema of 
the lower extremities, enlargement of the liver, cyanosis, etc., and the 
patient dies from asystole. In many cases complications are respon- 
sible for the final outcome—hemorrhage, which was already men- 
tioned, inanition due to laryngeal tuberculosis with dysphagia, amy- 
loid degeneration of the various visceral organs, etc. Tuberculosis 
of the previously unaffected lung may bring about a rapidly fatal 
course of the disease. 

I have observed that some of these cases, tuberculous in origin as 
they are, become purely bronchiectatic. The tubercle bacilli disap- 
pear from the sputum, but the patient continues to cough and expecto- 


428 FIBROID PHTHISIS 


rate large quantities of sputum which shows all the characteristics of 
sputum in bronchiectasis; in fact, the course is that of non-specific 
bronchiectasis after this occurrence. 

Prognosis in Fibroid Phthisis.— As regards duration of life, fibroid 
phthisis, though an active tuberculous disease and hardly ever cured, 
is more favorable than the other forms of phthisis, excepting abortive 
tuberculosis. It is among the fibroid patients that we find individuals 
who have been tuberculous for years. I have some who have lasted 
for twenty-five years, and Sokolowski reports one who lasted for more 
than forty years. While they are always ailing, many are still fit to 
pursue their vocations, and I have among my clientele some who have 
worked quite hard without long interruptions. 

In fibroid phthisis, the reparative processes of Nature are more 
active than the destructive tuberculous, and the patients are shielded 
from the extension of the caseating and softening processes, the 
fibrous tissue usually forming a wall around the lesion limiting its prog- 
ress and preventing the absorption of toxins, as is evident from the 
absence of fever, etc. Because of the pleural adhesions, the patients 
are shielded from such complications as spontaneous pneumothorax, 
which never occurs among them. When in my hospital practice I 
find a fibroid patient presenting the symptoms of spontaneous pneumo- 
thorax, it is soon clear that the rupture occurred in the lung which 
had been unaffected but recently showed a new lesion. 


Grin ER ee DLT 
ACUTE FORMS OF TUBERCULOSIS. 


As in other infectious diseases, there are observed in tuberculosis 
acute, malignant, or fulminating forms which run a shorter, and almost 
invariably fatal course. They are relatively rare, as malignant scarlet, 
measles, typhoid, etc., are rare. Every practitioner meets with 
these acute cases, and the laity is well aware of their existence. 
When tuberculosis makes its appearance in a member of a family 
anxious inquiries are made to ascertain whether it is not “hasty,” 
or “galloping consumption,” the names under which acute tuber- 
culosis is commonly known. Pathologically, the lesion is practically 
the same as that of the chronic forms of the disease, considering 
that there are no two cases of phthisis in which the anatomical changes 
are exactly alike, but clinically it manifests itself by a more rapid 
course, the patient lasting as many months with the acute form as 
years with the chronic forms. Acute pulmonary tuberculosis may be 
saud to be active chronie phthisis without the remissions and ameliorations 
characteristic of the course of the latter affection. 

It is unnecessary to enter into hair-splitting distinctions of the 
pathological and clinical types of acute pulmonary tuberculosis de- 
scribed by some authors. In practice we meet mainly with two types 
of the disease: The lobar pneumonic type—acute pneumonic phthisis, 
and the lobular, or bronchopneumonic type. In the former the 
patients are usually adults, while the latter attacks mainly infants 
and very young children, and adults only at the terminal stages of 
chronic phthisis. 

Between the two extremes—chronic and acute phthisis—there 
are many gradations; some are very acute, the patient being carried 
off within one or two weeks; some are subacute, lasting for two to 
four months, others even a year, but without any remissions in the 
progress. Then there are acute exacerbations during the course of 
chronic phthisis which are anatomically and clinically of the same 
character as the acute or subacute forms and often bring hitherto 
hopeful cases to a speedy termination. I have also met with cases 
which began acutely and kept up in that manner for several weeks, 
but suddenly, or ky degrees, took a turn for the better, and the patient 
passed through the course of chronic phthisis subsequently. 

Etiology.—The factors operative in causing an acute and malignant 
evolution of phthisis in some cases, while in the vast majority it is 
chronic, slow, and more or less benign, are not clear. From a careful 


430 ACUTE FORMS OF TUBERCULOSIS 


study of the cases met in practice it appears that the general condition 
of the patient before the onset of the disease has no influence in this 
direction. In fact, it appears, as will be shown later on (see p. 584), 
phthisis in those who suffered from scrofula, osseous, or glandular 
tuberculosis during childhood, or who are descended from tuberculous 
stock, is more likely to run a slow, sluggish course. On the other hand, 
we very often meet with acute phthisis in persons who have no heredi- 
tary taint, athletic individuals, who have been in excellent condition, 
and only rarely in the weakly and decrepit, excepting tuberculous 
bronchopneumonia in infants. 

The problem whether these acute cases are invariably due to more 
virulent strains of tubercle bacilli has not been solved, though there 
appears to be no evidence in favor of such a view. Some authors 
have held that acute phthisis is caused when a tuberculous cavity, or a 
caseating gland, breaks through into the lung, disseminating the secre- 
tions containing bacilli, but this is negatived by the fact that we meet 
numerous patients who never coughed before the onset of the acute 
disease. 

It appears that individuals who have never before been in tubercle- 
laden surroundings are more likely to develop acute phthisis when 
infected primarily after they have passed the age of childhood, as we 
have already shown (see p. 73). The same “virgin soil’ is presented 
by infants: when they are infected with tuberculosis they very often 
suffer from the acute forms of the disease, and so do adults hailing 
from rural districts where they have not met with tuberculosis, so 
that if infection takes place it is primary. The explanation of these 
phenomena has been discussed in a previous chapter. 


ACUTE FORMS OF PULMONARY TUBERCULOSIS. 


Acute Pneumonic Phthisis (Galloping Consumption.) —The anatomi- 
cal changes are those of pulmonary tuberculosis but the process of 
caseation and liquefaction gains the upper hand, not being limited by the 
conservative process of fibrosis which is a strong feature in chronic 
phthisis; little or no connective tissue is formed to localize the lesion. 
Usually the greater part of a lobe, or a whole lobe, is affected. The 
parenchyma is transformed into a solid, caseous, or gelatinous mass 
within which there can often be found a focus representing an old 
lesion. ‘The destruction of lung tissue goes on at a rapid pace, and 
within a short time more or less extensive excavations may be formed. 
But these excavations are not surrounded by a connective-tissue wall; 
all around them is caseated lung tissue. In many cases, however, 
death supervenes before softening has had time to set in to sequestrate 
the affected part of the lung. We may find scattered tubercles or 
caseous nodules all over the affected lung and also in the other, as well 
as on the visceral pleura, but pleural adhesions are rare, 


ACUTE FORMS OF PULMONARY TUBERCULOSIS 431 


Symptomatology.—The disease is niostly seen in adults between 
twenty and forty years of age. The onset and symptoms during the 
first few days are akin to those of lobar pneumonia. In fact, most of 
the cases of chronic phthisis which are said to have begun as lobar 
pheumonia are acute pneumonic phthisis which was not recognized 
as such at the onset of the acute stage. 

As given by the patients, the onset is nearly always acute. After 
some alleged exposure there was a chill, fever, pain in the chest, cough, 
etc. Buta careful inquiry elicits that while the acute symptoms have 
come on suddenly, the patient has for weeks, perhaps for months, 
felt out of sorts; was unable to perform his usual work without fatigue; 
in fact, he has coughed, expectorated and may have had some night- 
sweats. But these symptoms were not sufficiently pronounced to 
cause alarm; even if he has consulted his physician he may have been 
told that his troubles were trifling. This long prodromal stage is of 
great diagnostic importance, and will often aid while attempting to differ- 
entiate acute pneumonie phthisis from lobar pneumonia. 


























































































































Fia. 87.—Temperature curve in acute pneumonic phthisis. 


With the acute symptoms the patient is laid up in bed. The dyspnea 
is marked from the beginning, and may be paroxysmal. The pain in 
the side is mild, and only rarely as acute as in pneumonia or pleurisy, 
or may be altogether lacking. Cough is nearly always annoying; 
it may be severe, incessant, and exhausting. At first dry, it slowly 
becomes productive and the sputum is at times rusty and _ viscid, 
adhering to the sides of the vessel like in lobar pneumonia. But in 
most cases it is mucopurulent, frothy and easily brought up. In some 
cases it is sanguineous, at times repeated, small, true hemoptyses 
take place, and the disease may begin with a profuse pulmonary 
hemorrhage. When softening and excavation take place, which occur 
quite soon, the sputum is of the same character as that of chronic 
phthisis, excepting that it is more often green in color. In the begin- 
ning repeated microscopic examinations do not reveal any tubercle 
bacilli, and, because pneumococci are quite frequent, the diagnosis is 
very difficult. Only after the disease has lasted for a couple of weeks, 
and very often much later, when we may be thinking that we are dealing 
with an unresolved pneumonia, tubercle bacilli are discovered in the 
sputum, 


432 ACUTE FORMS OF TUBERCULOSIS 


Weakness, anorexia, emaciation, and fever are very strong clinical 
features in the evolution of the disease. The weakness may be so 
severe that very early in the course of the disease the patient is unable 
to sit up in bed, or to breathe deeply for the purpose of auscultation. 
When examined he falls back in bed exhausted, pale and cyanosed. 
This asthenia is not seen in the average case of lobar pneumonia. With 
the anorexia, which may be pronounced from the very beginning, 
emaciation goes hand in hand. Even in the cases in which the appetite 
is somewhat retained, the emaciation is very early and pronounced, 
and out of proportion to the fever and anorexia. It usually proceeds 
rapidly and often frightfully, so that within a few weeks a normally 
built man is reduced to a skeleton. Wasting is particularly quick in 
the muscles of the chest. More or less copious pulmonary hemorrhages 
may occur at any time. Some begin with a hemorrhage, as has already 
been stated. In others it occurs during the course of the disease, and 
now and then we meet with a case of acute pneumonic phthisis which 
succumbs to a profuse hemorrhage. 

In the beginning the fever is of a continuous type, like in lobar 
pneumonia, though some authors have described pneumonic phthisis 
without high fever, which I have never met in my practice. But this 
is rare during the first few weeks when the temperature curve ex- 
quisitely simulates that of lobar pneumonia, but during the second 
week, when we expect defervescence, we are disappointed. Instead 
of this, the fever becomes intermittent, or hectic, with morning remis- 
sions to normal or even below, and afternoon rises to 103° or 104° F., 
and accompanied by copious nightsweats. The pulse is rapid, small 
and feeble, and the blood-pressure low. The full, vigorous pulse of 
lobar pneumonia is never found. 

Physical Signs.— Physical exploration of the chest often shows the 
signs of typical lobar pneumonia. ‘There is impaired resonance or 
dulness over the upper part of one side of the chest above the third 
rib. But instead of the harsh tubular breathing, which is character- 
istic of pneumonia, we usually perceive diminished and, in some cases, 
complete absence of breath sounds, which are replaced by moist, sub- 
crepitant rales. The crepitation of pneumonia is only rarely audible. 
With the advance of the lesion the dulness becomes more pronounced 
and the respiratory murmur may be altogether abolished, or bronchial 
breathing may become audible coupled with small, and medium-sized 
moist rales. In acutely progressive cases signs of excavation may be 
found within four weeks; but this is rare. In many cases the lesion is 
centrally located, and the physical signs are indefinite. The writer 
has seen a case in which competent clinicians could not localize the 
lesion for about three months, when finally physical signs appeared 
over the upper lobe of the right lung. 

Course.—In most cases the acute symptoms persist for two or three 
months, the lesion softens, extensive excavations may form and the 
patient finally succumbs to asthenia. In some the process is of shorter 


ACUTE FORMS OF PULMONARY TUBERCULOSIS 433 


duration; I have seen cases in which death occurred in less than 
three weeks. In rare instances the disease is acute for four to six 
weeks, when an improvement in the general condition takes place and, 
with more or less extensive excavation in a lung, the patient becomes 
a chronic consumptive and the disease may even be arrested in time, 
which is, however, very rare. In some the toxemia is very severe, and 
the patient succumbs within two or three weeks, even before softening 
has taken place. The prognosis under the circumstances Is very grave, 
the average duration of the fatal cases, and they are in the vast major- 
ity, 1s about six weeks, dying from toxemia and exhaustion. I have 
seen several cases in which the end came through a brisk pulmonary 
hemorrhage. 

Differential Diagnosis.—It is often very difficult to differentiate 
acute pneumonic phthisis from lobar pneumonia, especially during 
the first two weeks of the ailment. Mistakes may be avoided by 
carefully inquiring for premonitory symptoms of tuberculosis pre- 
ceding the acute onset, such as anorexia, emaciation, weakness, mild 
cough, nightsweats, ete., which are frequent in acute phthisis, while 
in lobar pneumonia the patient is stricken suddenly when he feels in 
the best of health. In fact, in apical pneumonia, and in pneumonia 
following an atypical course, acute tuberculosis is always to be thought of. 
The absence of pain in the side, the late arrival of true bronchial breath- 
ing, the hemoptysis, etc., may all lead to a diagnosis, or at least a 
suspicion of acute phthisis. An irregular temperature curve, mild 
dyspnea, severe pallor, low leukocyte count, absence of pneumo- 
cocci from the sputum, and a strong diazo-reaction may algo be con- 
sidered. Of great importance in favor of acute phthisis is yellow or 
green sputum. ‘Tubercle bacilli are conclusive evidence, but they are 
only rarely found before the end of a month. On the other hand, in 
lobar pneumonia complicating pulmonary tuberculosis, we may find 
tubercle bacilli in the sputum. Several cases of this type have come 
under the writer’s observation, and a diagnosis of acute pneumonic 
phthisis was made, and within a week or ten days the pneumonia ended 
by crisis, while the tuberculous disease subsequently pursued its course 
unaffected by the pneumonic complication. However, these com- 
plicating pneumonias, as a rule, attack one of the lower lobes, and this 
fact should be considered in all cases. During the first week the 
emaciation is negligible in pneumonia, irrespective of the acuteness 
of the symptoms, while in phthisis it is immediately pronounced; 
nightsweats, weakness and edema of the lower limbs are frequent. 
The crisis, which is sure to come before the fourteenth day in the vast 
majority of cases of pneumonia, will clear up doubtful cases. 

Especially difficult is the diagnosis of pneumonic phthisis in aged 
persons, in whom it may occur without much fever and other general 
symptoms, and only positive sputum can decide. 

Tuberculous Bronchopneumonia.—Etiology.—The anatomical changes 
in tuberculous bronchopneumonia are those of pulmonary tuberculosis, 

28 


434 ACUTE FORMS OF TUBERCULOSIS 


excepting that the lesion is not localized in one apex, or one lobe, but 
disseminated all over one or both lungs in which there are distributed 
caseous nodules which vary in size from that of a pin-point to that of 
a walnut. Some authors have been inclined to attribute the wide 
dissemination of the lesion, as well as the acute course of this form of 
tuberculosis, to mixed infection with tubercle bacilli and pyogenic 
microdrganisms. This, they believe, is confirmed by the fact that it 
very often follows other infections such as measles, whooping-cough, 
influenza, typhoid, ete., showing that the patient had harbored a tuber- 
culous process before, but with the addition of a new infective agent 
his vitality was reduced and the tuberculous process allowed to spread 
all over the lungs. But against this view may be brought forward the 
numerous cases in which mixed infection can be positively excluded. 
Moreover, as will be shown elsewhere, in cases in which typhoid fever 
or influenza is supposed to have preceded the tuberculous disease, 
careful investigation usually reveals that the acute initial symptoms 
were those of tuberculosis, but an erroneous diagnosis was made of 
some other infection. 

In most cases it appears to be the result of the wide dissemination 
of the contents of a tuberculous cavity in the lungs, or the perforation 
of a tuberculous lymph node, the contents of which are aspirated, 
carried all over the bronchial tree and take root in various parts of the 
lungs. In infants, among whom this form of the disease is very com- 
mon, it may be due toa primary massive infection with tubercle bacilli; 
the body possessing no immunity through previous infection, the 
result is the same as when a guinea-pig is infected. In adults, we also 
meet it iff women after childbirth, in tuberculosis with diabetes and 
alcoholism, etc., and more commonly, as a terminal phenomenon of 
chronic phthisis when the resisting powers are at low ebb, and immu- 
nity acquired by the existing lesion is lacking. 

Symptoms.—Tuberculous bronchopneumonia in adults is usually 
found in patients who have been tuberculous for some time. In 
those in whom it appears to be of sudden onset, careful inquiry elicits 
the information that the patients have been ailing for some time with 
symptoms highly suggestive of tuberculosis. In fact, it is often a 
complication of chronic phthisis: A patient who has been doing 
fairly well suddenly develops acute symptoms without any special 
cause; more often after a surgical operation in which a general anes- 
thetic was employed. Tuberculous women are, at times, the victims 
soon after childbirth. 

The clinical picture is that of an acute infectious disease with pro- 
nounced toxemia. The onset is sudden, often with a chill, fever, 
backache, cough, expectoration, etc. The fever is usually high— 
103° to 104° F. is not uncommon—and in children it may be even 
higher. The temperature curve is not characteristic; in fact, it may 
be stated that its peculiarity is its irregularity. In many cases it 
is continuous with slight remissions, but in others it is intermittent, 


ACUTE FORMS OF PULMONARY TUBERCULOSIS 435 


with chills before each rise. During the terminal stages it is usually 
hectic. The sweats are profuse and exhausting, the pulse feeble, 
small and rapid, 120 to 150 is not rare; the dyspnea is marked—40 
to 60 per minute are very often counted, and cyanosis is a frequent 
feature. Graves spoke of “acute tubercular asphyxia.”’ 

The intensity of the cough is variable: In some patients it is severe, 
painful, paroxysmal, and may provoke vomiting. While occasionally 
the cough is mild, in most cases it is more severe than in chronic 
phthisis. At times expectoration is absent or scanty, but usually it 
is more or less abundant, often purulent, and, with the advance of the 
disease, nummular; yellowish-green balls are brought up. ‘Tubercle 
bacilli are found in most cases. 

Hemoptysis is frequent in adults and may be quite copious; many 
cases begin with pulmonary hemorrhage. 

The appetite is rarely fairly well retained, but in most cases this, 
as well as the digestive functions, 1 is impaired; many have to be coaxed 
to take some nourishment. Emaciation proceeds at a rapid pace. 


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Fic. 88.—Temperature curve in tuberculous bronchopneumonia. 


Because of the flushed face it is at times not appreciated at first sight, 
but when the bedclothes are removed, the marked wasting of the 
subcutaneous tissues and muscles of the chest and extremities presents 
a frightful picture, especially when it is considered that it may have 
been consummated within a few weeks. 

Physical Signs.—The physical signs vary according to the nature 
of the anatomical changes in the lungs. In the beginning they may 
be obscure and misleading. In most cases the note elicited on per- 
cussion is hyperresonant all over the two sides of the thorax; localized 
dulness is found only later when some of the disseminated tubercles 
have become confluent. Auscultation shows either feeble breathing 
or harsh bronchovesicular breath sounds all over the chest, coupled 
with sibilant and sonorous rales. With the advance of the disease, 
which may be within but one or two weeks, we find localized areas, 
not necessarily in the apex, especially in children, of consolidation 
with bronchial breathing and moist subcrepitant rales which soon 
change their character when excavation takes place and the usual 
signs of a cavity can be made out. In many cases, notably in children, 


436 ACUTE FORMS OF TUBERCULOSIS 


signs of diffuse bronchitis are found all over the chest, while in others 
the toxemia is so severe that the patient succumbs before definite 
changes in the resonance and breath sounds have developed. 

Complications. Among these may be mentioned pulmonary hemor- 
rhage, which may be fatal; intestinal tuberculosis, tuberculous menin- 
gitis, and general miliary tuberculosis. 

Diagnosis.—The diagnosis is very difficult in the initial stages, 
particularly in children, among whom it must be differentiated from 
postgrippal bronchopneumonia, and sputum is not available for 
microscopical examination. In adults it is usually more easily diag- 
nosticated. We find in patients who have been tuberculous for some 
time that after a hemorrhage, surgical anesthesia, pregnancy, etc., 
the symptoms suddenly fake a sharp turn and galloping consump- 
tion follows. It is alws ays to be borne in mind that when in a person 
who never before had emphysema, and who has no barrel-shaped chest, 
symptoms and signs of emphysema suddenly make their appearance 
accompanied by acute constitutional symptoms such as fever, cough, 
dyspnea, cyanosis, nightsweats, etc., acute phthisis is to be thought of. 
The sputum will soon clear up the diagnosis. With the advance of 
the disease the physical signs are easily made out. 

Prognosis.—The prognosis is very grave. Some acute cases run 
a rapid course, terminating fatally within four to six weeks, and in 
children in a shorter time. Many cases linger for three or four months, 
and die of asthenia. I have met some cases in which the disease came 
to a halt and assumed the character of chronic phthisis. 


ACUTE MILIARY TUBERCULOSIS. 


Pathogenesis.— When from an existing tuberculous focus anywhere 
in to body a large number of tubercle bacilli are released into the blood- 
r ly mph-stream, a bacteremia results, the microdrganisms settling 
in hic various visceral organs producing small tuberculous nodules. 
In this form of acute tuberculosis most of the viscera are affected, 
while in the acute forms of pulmonary tuberculosis, which have just 
been described, or in the various forms of tuberculosis of the glands, 
serous membranes, bones, or joints, only the affected tissues bear the 
brunt of the infection. 

Acute miliary tuberculosis is hardly ever primary; in nearly all cases 
there had existed a localized tuberculous focus which may have been 
small, hardly detectable at the autopsy, and which may have given no 
symptoms during the life of the patient. But when a bloodvessel 
passing through, or in contact with, a caseated lymphatic gland, or a 
caseated area of any tissue, erodes; or when a tubercle involving the 
wall of a vessel softens, and produces ulceration of the intima, large 
numbers of tubercle bacilli are set free into the circulating blood. 
Similar effects will be produced indirectly when the thoracic duct is 


ACUTE MILIARY TUBERCULOSIS 437 


affected by tuberculosis, and bacilli enter through the subclavian vein 
into the general circulation. 

It is, however, rare that a caseated tuberculous area should break 
into the circulation directly. The most common mode appears to be 
the formation of tubercles in the walls of a vessel, especially the 
pulmonary vein, or the thoracic duct. Benda! found metastatic 
tuberculous endangeitis more common than periangeitis. When these 
tubercles soften, breaking through the endothelial lining, a constant 
stream of tubercle bacilli enters the circulation. Its occurrence is 
comparatively infrequent, because tuberculous endangeitis is relatively 
rare owing to the fact that in the usual tuberculous lesion the blood- 
vessels within, and in the neighborhood of, old foci are thickened as a 
result of the inflammatory reaction, their lumen is obliterated, and 
thus erosion and passage of tubercle bacilli into the blood stream is 
prevented. Otherwise the vast majority of cases of tuberculous 
infection would implicate bloodvessels and lymphatics in and adjoining 
the lesions, and acute miliary tuberculosis would result. 

It must, however, be emphasized that a tuberculous bacteremia 
is not sufficient to produce acute miliary tuberculosis; excepting in 
cases of primary massive infections which occur in infants, as has been 
shown elsewhere. In adults with chronic tuberculous lesions, among 
whom primary tuberculous infection is, as a rule, out of the question 
for reasons already stated, tubercle bacilli are very often found in the 
circulating blood, yet no miliary tubercles are formed in the visceral 
organs. It seems that before the body can be overwhelmed by 
tubercle bacilli and permit them to produce miliary tubercles in the 
various viscera, some factors which reduce the natural resisting forces 
must be at work, the blood must have lost its normal bactericidal 
powers, to permit the bacilli in a virulent state to settle anywhere they 
please. In the usual case of local tuberculosis the bactericidal action 
of the blood is effective in either killing the organisms, or at least in 
attenuating their virulence, so that even animal inoculation of blood 
containing acid-fast bacilli proves harmless (see p. 285). 

What these etiological factors are, we do not know, and when they 
are elucidated, the most important problems in the pathogenesis of 
tuberculosis will be cleared up. In many tuberculous patients with 
active disease, acute miliary tuberculosis appears as a terminal phe- 
nomenon. In others, with healed or arrested lesions, symptoms of 
acute miliary tuberculosis appear leading to a fatal issue after chilling 
the body, after surgical operations, especially for some extra-thoracic 
tuberculous lesion, or without any obvious exciting cause. In hospitals 
for tuberculous patients there are at times to be observed “epidemics” 
of acute miliary tuberculosis. This is especially seen during changeable 
meteorological conditions, or when intercurrent infections are common. 
It may also occur after a pleural effusion is rapidly absorbed, or 
aspirated. 

1 Ergebn. d. allg. Pathol., 1900, 5, 447. 


438 ACUTE FORMS OF TUBERCULOSIS 


, Evidently because tuberculous infection is primary in infants, when 
massive, it may result in acute miliary tuberculosis; it usually follows 
some intercurrent infection, as measles or pertussis. But it is not as 
rare in adults as some believe. A large proportion of fatal cases of 
chronic phthisis are carried off by symptoms and acute miliary tuber- 
culosis which make their appearance at the end. It has been suggested 
that the accessible and wide lymphatic system of infants offers better 
opportunities for the bacilli to enter the lymph glands, and after these 
soften, they pass into the thoracic duct, finally reaching the general 
circulation and then disseminating throughout the body. 

Pathology.— Miliary tubercles are found in most of the visceral 
organs. ‘The lungs, as the locus minoris resistenti@, contain more than 
other organs, but the spleen, liver, kidney, also the thyroid, bone- 
marrow, the heart, meninges, peritoneum, choroids, etc., may be 
studded with miliary and submiliary tubercles. These nodules are of 
various sizes, according to their age and density of conglomeration; 
young ones are small, hardly visible, at first gray and transparent, but 
later many adjoin one another and caseation begins, when they appear 
yellowish. In each organ tubercles of various ages may be discerned 
owing to repeated migration of bacilli from the original focus which 
settle wherever they find a suitable soil. The surface of the affected 
organs, as well as the large serous membranes, may be found sprinkled 
with these nodules. In most cases the old original tuberculous lesions, 
the source of the bacilli which overwhelmed the body, may be dis- 
covered in the lungs or glands. In adults, in whom acute miliary 
tuberculosis was a terminal phenomenon of chronic phthisis any kind 
of tuberculous changes may be found in the lungs, pleura, peritoneum, 
larynx, intestine, etc. 

Symptoms.—The manifold origin, and different localization of the 
main clusters of tubercle within the visceral organs result in a variegated 
symptomatology of acute miliary tuberculosis. In cases which the 
tubercles are scattered equally among these organs, the symptoms are 
not unlike those of other forms of acute general infections, as septicemia, 
or typhoid fever; in fact a typhoid form of acute miliary tuberculosis 
has been described. In cases in which tubercles are sprinkled over the 
meninges, cerebral symptoms predominate and may overwhelm the 
clinical phenomena. We thus have a meningeal form of miliary 
tuberculosis. In some cases the lungs bear the brunt of the infection, 
pulmonary symptoms are then in the ascendency, producing the pul- 
monary form of the disease. However, it must be emphasized at the 
outset that mixed forms are very frequently met with, or one form 
passes into another; the typhoid and pulmonary forms very often 
present symptoms of the meningeal form at the end. Consequently, 
no sharp line of demarcation can be drawn between these three clinical 
forms of the disease, and it is merely for descriptive purposes that this 
division is followed. 


ACUTE MILIARY TUBERCULOSIS 439 


The Typhoid Form.—The onset may be sudden without any pre- 
monitory symptoms. The patient may have considered himself well, 
never having known of any tuberculous lesion in his body, or he may 
have had some slight cough for years which was known to be of tuber- 
culous origin, but he has been pronounced cured. He may have been 
tuberculous for months or years, and properly treated, the disease 
pursuing a favorable course, ete., when suddenly, after some exposure, 
or without any assignable cause, he has a chill, his temperature rises, 
and he presents symptoms of a profound intoxication. The fever 
rises to 103° F., or higher, within one or two days, the pulse is rapid, 
small, and soft, the blood-pressure low, and other symptoms of toxemia 
make their appearance—dry, coated tongue, anorexia, dyspnea, etc. 
Delirium may be an early symptom, or it may appear toward the end. 
While constipation is not rare, in some cases there is annoying diarrhea 
and this, with scattered roseola over the body, and a large spleen, 
point to typhoid fever which is often diagnosed especially in patients 
who had no symptoms of tuberculosis before the onset of the acute 
process. 

Physical exploration of the chest may prove negative, or signs of a 
disseminated bronchitis may be elicited. But a careful study of the 
symptoms and course shows the real condition. Thus, a characteristic 
fever curve of typhoid is lacking; instead of high continuous fever, 
we may have a remittent curve, which later becomes intermittent. In 
many cases the fever curve is altogether irregular, for a few days it is of 
one type, then of another. Rarely the “reverse” type (see p. 222) is 
observed. ‘The emaciation is rapid and pronounced, dyspnea and 
cyanosis are more severe than in the average case of uncomplicated 
typhoid. Then cerebral symptoms make their appearance: rigidity 
of the neck, differences in the pupils, evidences of palsies, especially of 
the cranial nerves, etc., and within two or three weeks a fatal termina- 
tion occurs. 

The Pulmonary Form.—Here the conglomeration of tubercles 
predominates in the lungs; not only one or more lobes are mainly 
affected, as is the case in acute pneumonic phthisis, but nodules are 
scattered all over both lungs. The symptoms are those of profound 
toxemia with signs of pulmonary disease. The patients may have 
coughed for some time, or may have been known as tuberculous for 
months or years. In rare instances no such history is obtained. The 
temperature rises, and within two or three days it reaches 104° F., or 
higher. In old persons it may be lower, and in some cases it hardly 
exceeds 99.5° F. With the fever there is profuse sweating, not only 
during the night, but also during the day. In some instances the 
disease begins with a chill, and chilly sensations may occur several 
times a day during the course of the disease, the chills being followed 
by a rise in the temperature, and then by profuse sweating. In some 
cases, especially at the end, there is observed an intermittent tempera- 
ture, with subnormal, or even collapse, temperature in the early morn- 
ing hours. . 





440 ACUTE FORMS OF: TUBERCULOSIS 


Symptoms referable to the respiratory system are present in nearly 
all cases. In some instances cough may be altogether lacking during 
the first week of the disease, but in most there is a dry hacking cough, 
and paroxysmal attacks of great severity are not rare. Usually the 
cough is unproductive early in the disease, excepting in those in whom 
the acute process is superimposed on an old phthisical condition. 
The sputum brought up is not characteristic and, as a rule, does not 
show the presence of tubercle bacilli. Streaks of blood may be observed 
in the sputum, and rusty sputum, without any evidences of pneumonia, 
is seen in rare instances. In patients with old tuberculous lesions 
there may occur copious, or even fatal, pulmonary hemorrhages, while 
in those in whom the acute process complicates chronic phthisis acute 
miliary tuberculosis may follow a brisk hemorrhage. But this is rare. 

Dyspnea and cyanosis of the lips and finger tips are seen in most 
cases very early, and this is important diagnostically. The breathing 
is superficial and rapid, 50 to 80 per minute; in some cases orthopnea 
is observed. In patients without pronounced old lesions, exploration 



















































































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Fig. 89.—Temperature curve in acute miliary tuberculosis. 


of the chest may reveal nothing definite, or some small, moist rales may 
be audible over any part of the lungs; in others sibilation in either, or 
both, sides is heard. Percussion does not bring out any localized areas 
of consolidation, but tympany may be found all over, in on some 
parts, especially the upper third of the chest, dulness with a tympanitic 
overtone, owing to the relaxation of the parenchyma because of the 
dissiminated nodules within them. Here and there some moist rale 
is made out, and friction sounds may be audible over the lower parts 
of the chest. In many cases symptoms and signs not unlike those of 
pulmonary emphysema are elicited. On the whole, there is a striking 
discordance between the severity of the constitutional symptoms 
and the paucity of the physical signs, and this is of diagnostic 
significance. 

With the advance of the disease, which may continue for four to 
eight weeks, and rarely longer, symptoms of the typhoid form, and of 
meningeal irritation, make their appearance, and the end comes either 
from exhaustion and collapse with a subnormal temperature, or, more 
commonly, with high fever, delirium and meningeal symptoms. 


od 


ACUTE MILIARY TUBERCULOSIS 44] 


Meningeal Form.—This is most frequently seen in children, but in 
adults with known tuberculous lesions in any organ which have lasted 
for some time, it is a not very uncommon mode of death. About 5 
per cent of patients with pulmonary tuberculosis succumb finally to 
tuberculous meningitis. Metastasis in the meninges is more likely to 
occur in cases of extra-pulmonary lesions, active or latent. Thus, as 
is shown elsewhere, it is very frequent in genito-urinary tuberculosis 
in adults, and in children with osseous, glandular and articular tubercu- 
losis. In infants, however, it often follows tuberculous broncho- 
pneumonia. But here also the intrathoracic glands are severely 
affected, as a rule. The general infection occurs hematogenously, 
but it may also take place lymphogenously. 

Symptoms in Children.—In children the onset may be abrupt, with 
persistent vomiting or convulsions. But in such cases, if carefully 
looked for, a chronic tuberculous process in some glands may be found, 
though it may not have been inconsistent with apparent health of the 
child. More frequently it was known for weeks or months that the 
child was sick. It may have been coughing, but this was attributed 
to some mild disorder in the throat or bronchi; it may have had some 
recognized tuberculous gland on the neck, or within the chest, or a 
tuberculous lesion in a bone or joint. But all this was considered 
trifling. The child, however, kept on losing ground, its appetite has 
been poor, and it has lost, or failed to gain, in weight. Its mental 
state has become rather peculiar, it has been out of sorts, refused to 
play, sought seclusion, complained of headache, avoided bright light 
and loud noises. Constipation is the rule, but in some the reverse is 
true. In few, attacks of vomiting, at times of the projectile type, 
may be observed at this stage. Careful thermometry will reveal a 
mild subfebrile temperature. 

This prodromal stage may last for several weeks, but in most cases 
within two or three weeks, symptoms pointing to the cerebral nervous 
system make their appearance, such as a slight facial palsy, a squint, 
cutaneous hyperesthesia, erythematous blotches, dermographism, 
stiffness of the neck, etc. In some instances palsy of a limb is noted 
at this stage. The child becomes drowsy, responds only when strongly 
urged. The pupils may be normal, or contracted, but they respond to 
light. In some, nystagmus is seen at this stage. The reflexes are 
exaggerated. Spastic contraction of the muscles, especially those of 
the spine, is common, the neck is rigid and drawn back, and later 
opisthotonos may occur. Kernig’s sign is present in nearly all cases. 
Later on the spasticity may become more accentuated on one side, and 
there may occur paralysis of an arm or leg, and of some of the cranial 
nerves, especially the facial and oculomotor. The pupils now cease 
to respond to light, and inequality is not uncommon. Delirium, 
frequent in adults, is rare in children; they are usually in stupor from 
which it is hard, or impossible, to arouse them. Convulsions may now 
become more and more frequent, or coma supervenes. ‘The vaso- 


449 ACUTE FORMS OF TUBERCULOSIS 


motor disturbances now become more and more pronounced, tache 
cérébrale is hardly ever absent. The pulse, which may have been 
rather slow in the beginning, now becomes rapid and irregular. 

As is the case in adults, remissions may occur, and false hopes are 
thus engendered when the stuporous child wakes and acts quite nor- 
mally for a few hours, a day or two. But arelapse is sure to occur, the 
symptoms return with greater severity, and within one to three weeks 
the stupor passes into coma from which the child cannot be aroused 
and, with Cheyne-Stokes breathing, convulsions, hyperpyrexia, etc., 
the child expires. 

Symptoms in Adults.—Many phthisical patients show cerebral 
symptoms a few days before death, but at the autopsy no changes are 
found within the cranium. In these cases the diagnosis is not very 
important because the seriousness of the condition is evident from 
the other symptoms. The problem of the presence or absence of 
meningeal tuberculosis in phthisical patients has, however, a great 
prognostic value in cases showing a tendency to quiescence or cure, and 
the occurence of symptoms suggestive of tuberculous meningitis is 
more than disquieting. 

In most cases the onset is insidious. For some days, at times for 
more than two weeks, the patient complains of headache. Tuber- 
culous patients, even when they run fever, only rarely suffer from 
headache lasting more than a day or two, and then it is due to the 
pyrexia, or gastro-intestinal trouble. Acute rhino-pharyngeal inflam- 
mation may be the cause of headache, but this also is rare in tuber- 
culous individuals. If headache lasting several days, which cannot be 
explained as due to some evident cause, occurs in a phthisical patient, 
meningitis is to be thought of. Vomiting is extremely rare in the early 
stages of tuberculous meningitis in adults. More common prodromal 
symptoms are irritability, fretfulness, confusion of ideas, impaired 
memory, photophobia, defective vision, drowsiness, and somnolence. 
In some, symptoms not unlike those of classical hysteria are observed 
for several days, and when occurring in a patient who had no such 
stigmata before, especially in males, hysterical manifestations are sug- 
gestive of meningeal irritation by tubercles. 

The pulse-rate, which may have been accelerated, becomes slow in 
many, though not in all cases, and in some irregularity occurs. The 
temperature is high in some instances, but in most it hardly exceeds 
102° F. I have seen instances in which the temperature was normal, 
or even subnormal. Constipation may occur even in those who had 
diarrhea. Another early symptom is retention of urine which, when it 
does occur, is of immense diagnostic value. 

An important feature is a sudden change of character—the hopefulness 
and euphoria, which may have been more or less pronounced, change 
into indifference; the patient ceases to ask for relief, ceases to complain 
about the treatment given him, loses interest in his surroundings, 


ACUTE MILIARY TUBERCULOSIS 443 


and-lies in a semi-stuporous state unless waked, and then only answers 
questions abruptly. 

In most of the cases under the writer’s observation these symptoms 
occurred early, but it is important to mention that, as a rule, they were 
not continuous; occurring one day and disappearing the next, to reappear 
again. ‘This intermittency is a very important point in the diagnosis 
of obscure cases. I have known cases in which the symptoms de- 
scribed above lasted about a week, then disappeared, the patient feel- 
ing quite well for one or two weeks, to relapse again when clear and 
unequivocal symptoms of tuberculous meningitis prove fatal. 

During this stage some signs characteristic of this disease may be 
discovered. In most, Kernig’s sign may be positive very early, 
though it is usually discovered later on. At times slight palsies, 
especially of the cranial nerves, may be noted when carefully examining 
the face. Transient monoplegia of an arm or leg occurs at times, In 
others, complete hemiplegia. Likewise aphasia occurs in some cases 
either as a transient phenomenon, or remaining to the end. Hyper- 
esthesia, mainly of the muscles, is very common; so is dermographism. 
The pupils usually react to light and accommodation during the 
prodromal stage, but later on a defect in this regard is observed and 
there may be unilateral or bilateral ptosis, converging strabismus, and 
only rarely diverging strabismus. In some nystagmus occurs. An 
ophthalmoscopic examination may reveal tubercles in the choroid, 
which is conclusive as to the diagnosis. 

Extensive experience has taught me not to rely implicitly on the 
results of lumbar puncture for diagnostic purposes in these cases. In 
most cases the fluid is found to come out at a high pressure, usually 
it is clear, in rare instances it is cloudy, rarely sanguineous, and often 
shows an excess of lymphocytes. But it must be mentioned that an 
excessive number of lymphocytes is not invariably a sign of tuberculous 
meningitis. It has been found in patients who did not develop the 
disease, while in many fatal cases with autopsy proof of tuberculous 
meningitis, no changes in the cerebrospinal fluid and its cytology 
could be found during life. Very frequently tubercle bacilli are found 
in the fluid. Excepting positive bacteriological findings, the writer 
would not make a diagnosis of tuberculous meningitis merely because 
of the high pressure, and the cytology of the cerebrospinal fluid alone, 
unless the symptoms are decidedly confirmatory. 

Within a week or two after the onset of the prodromal symptoms the 
patient sinks into a stuporous condition, then into coma from which 
he can be waked with difficulty, and then the coma deepens until the 
end. Convulsions may occur, though this is comparatively rare. 
Retention of urine is very frequent during the last few days. A fatal 
prognosis should be given wherever meningitis is diagnosed; the few 
cases of recovery which have been reported! may be considered medical 
curiosities. 

1 See Harbitz: Am. Jour. Med. Sci., 1921, 161, 212, 


+44 ACUTE FORMS OF TUBERCULOSIS 


Diagnosis.— Acute miliary tuberculosis is not a disease which can be 
easily diagnosticated. When occurring in apparently healthy persons 
it is very often mistaken for some other acute infection, notably 
typhoid fever, septicemia, bronchitis, bronchopneumonia, malaria, 
etc. When attacking a patient who had been phthisical, the acute 
disease is at times considered by the attending physician as merely an 
acute exacerbation of the localized pulmonary lesion and a hopeful 
prognosis is rendered. In hospitals for advanced tuberculous patients 
the disease is more often suspected than it actually occurs. 

It has been an ancient diagnostic principle to think of acute miliary 
tuberculosis in all cases of fever lasting more than a week and which 
cannot be diagnosticated as due to some other cause. In most cases 
it may be elicited that the onset was not as sudden as the patients 
claim, but that for weeks perhaps for more than a month, they have 
been feeling out of sorts, lost in weight, coughed mildly, perspired at 
night. In many, there will be found signs of a tuberculous lesion, 
active or latent, somewhere in the body; special inquiry should be made 
for symptoms and signs of tuberculosis of the pleura and the genito- 
urinary organs. In children the glands should be carefully examined. 

The fever curve alone is not characteristic of the disease, though if 
watched for several days it may give some criterion. The lack of type 
in the fever, one day high, the next low, intermittent, or remittent, 
may help in excluding typhoid, pneumonia, malaria, etc., but the fever 
curve in septicemia often shows similar characteristics, while in acute 
miliary tuberculosis it may be continuous for a week, or more. More- 
over, When complicating active pulmonary tuberculosis the fever curve 
may be the same as it had been before the onset of the complicating 
acute miliary tuberculosis. In senile patients the course may be 
altogether afebrile. Cornet observed such cases in young adults, and 
he concludes that it is a sign of cardiac weakness. The duration of the 
fever is at times misleading, because there are cases of miliary tuber- 
culosis which last for several months, and only when cerebral symptoms 
make their appearance is the true condition recognized. 

While with the meningeal implication the pulse may be slow, 
especially in children, it is rapid, soft and compressible in all other 
forms of the disease. The low blood-pressure may be of assistance at 
times. But the enlarged spleen, which is quite common, may lead one 
to suspect typhoid fever. Increase in the number of neutrophile poly- 
nuclears in the blood, diminution in the number of lymphocytes, and 
lack of eosinophiles, which are otten observed, are of little diagnostic 
assistance in cases complicating chronic phthisis because this blood 
picture is common in cases of active phthisis without miliary complica- 
tion. This blood picture is also often found in septicemia, and in 
pneumonia, though in the latter an absolute increase in the number of 
leukocytes is almost invariably observed. When, in an obscure case, 
there is observed an increase in the polynuclears, combined with leuko- 
penia, acute miliary tuberculosis is to be considered likely. The 


ACUTE MILIARY TUBERCULOSIS 445 


diazo-reaction is positive early, and persists throughout the disease, 
while in typhoid fever, it becomes positive only during the third or 
fourth week. ‘Tubercle bacilli in the blood may be found in chronic 
as well as in acute miliary tuberculosis. However, a positive Widal 
reaction Is rare in miliary tuberculosis. While in some cases tubercles 
may be seen in the choroid on careful and competent ophthalmoscopy, 
some authors even saying that this is true in 80 per cent of cases, this 
is a late clinical phenomenon, when other symptoms are decisive. 
Post mortem they are very commonly found. 

After excluding typhoid fever, pneumonia, septicemia, etc., in a 
case of prolonged fever acute miliary tuberculosis is to be considered. 
When there is a rapid pulse, severe dyspnea, cyanosis, and a hacking, 
unproductive cough without any conclusive symptoms and signs of 
cardiac or pulmonary disease, the suspicion rests on a firmer foundation. 
In most cases it is the disharmony between the severe constitutional 
symptoms, with the negative findings in the chest, that leads to a diag- 
nosis. In patients with pronounced tuberculous lung lesions, the sud- 
den onset of higher fever, dyspnea, and cyanosis, when not due to 
pleurisy or pneumothorax, suggests complicating miliary tuberculosis. 

Roentgenography.— When well developed, the lesions of acute miliar y 
tuberculosis of the lungs are easily detected with the aid of a ood 
roentgen plate. As was already stated, single tubercles cast no distinct 
shadows; only when several tubercles Sane in one spot that 
they produce a round or oval shadow which i is more or less charac- 
teristic. These spots are seen scattered all over the pulmonary fields, 
more densely over the upper lobes, and at the roots of the lungs. Each 
spot represents a conglomeration of tubercles. In appearance they 
have been compared with a thick snowstorm. In some places these 
foci conglomerate more densely and produce an opacity on the plate 
which is much larger than the rest of the foci. In some cases the 
individual foci are not at all visible on the plate because the entire 
pulmonary field is opaque owing to the small size of each individual 
tubercle, and their larger number, and also because of the pulmonary 
edema which is a concomitant of this form of miliary tubercle. Cloudi- 
ness of the pulmonary field is the only thing that may be observed in 
these cases. 

Though characteristic, these scattered foci should not decide in favor 
of miliary tuberculosis when the constitutional symptoms are not in 
agreement. Plates taken in cases of pneumokoniosis show pictures 
exactly like those of miliary tuberculosis, and the most expert is likely 
to be deceived. This has been a source of error which led astray many 
roentgenographers. It strikes me that the following points may assist 
in differentiation of such plates: In pneumokoniosis these foci are, 
as a rule, irregularly distributed all over the lung fields, especially in 
the region of the roots of the lungs where the glands retained the dust, 
and each spot differs materially in appearance and size from the others, 
while in miliary tubercle they are nearly all alike in size and appearance 


446 ACUTE FORMS OF TUBERCULOSIS 


and there is a tendency to segregation in the upper parts of the lungs. 
However, in advanced miliary tuberculosis the conglomeration of 
tubercles may also produce larger foci in some places on the plate. 
This again shows that only the constitutional symptoms decide. 

Another difficulty in diagnosis arises at times. A patient with 
pneumokoniosis develops a tuberculous lesion which is localized and 
circumscribed, perhaps even fibroid in character, and the prognosis 
is quite favorable. A roentgenographic plate is made and disseminated 
foci all over the lung fields are observed in addition to the localized 
lesion in one of the apices and a diagnosis of miliary tuberculosis is 
made. In such cases a history and clinical observation for some time 
decides. 

Miliary carcinomatosis, when hematogenous metastasis has taken 
place, produces a roentgen picture of the chest which cannot be dif- 
ferentiated from that of miliary tuberculosis. I have seen two cases 
in which this difficulty had arisen and it took some time before it could 
be cleared up. Usually the original neoplasm in some of the abdominal 
viscera, the thyroid, ete., can be found clinically, but now and then the 
diagnostic difficulties are perplexing. 

Course. —The course of the disease is nearly always to a fatal termina- 
tion. This may be expected within three or four weeks, but in rare 
instances it has been observed to last for several months. I have had 
cases in the hospital that lasted four and even six months, finally 
succumbing to meningeal implication. Even the meningeal form, in 
rare instances, lasts more than a month, with several remissions, 
apparently indicating that an error had been made in diagnosis, but 
within a few days, in one case after two weeks, the symptoms of 
meningeal irritation returned and the patient died. Cornet mentions 
instances in which the period of remission lasted over a month. 

Patients presenting symptoms of the pulmonary form of the disease 
often go into the typhoid state and die in coma. Many show symp- 
toms of edema of the lungs during the last few days, while convulsions 
are rare in adults. There have been reported cases of acute miliary 
tuberculosis which recovered, even such as showed tubercle bacilli 
in the cerebrospinal fluid, yet this is so extremely rare that it is not to 
be considered after the diagnosis has been positively made. Some 
last for months, as has been stated, and some authors have spoken 
of chronic miliary tuberculosis. In these cases several diagnoses have 
been made before the patient showed finally symptoms and signs of 
the typhoid, or meningeal, form of miliary tuberculosis. 


GHA Pl HE Re xx TV: 
PULMONARY TUBERCULOSIS IN CHILDREN. 


General Characteristics of Tuberculosis in Children.—In children 
infection with tubercle bacilli, if it causes active disease at all, is 
usually followed by a generalized morbid process with implication of 
the lymphatic glands. This characteristic is the more accentuated 
the younger the child. In fact, in all infectious diseases we may note 
that the reaction of the lymphatic glands is intense in children. The 
glands are particularly sensitive to tuberculosis, and it appears that 
during infancy they are unable to retain the organisms, but permit 
them to spread all over the body. 

The localized disease of the lungs peculiar to phthisis in adults, 
or in the bones and joints, characteristic of early childhood, is only 
rarely seen ininfants. In infants tuberculosis is an acute, general infec- 
tion, like typhoid or septicemia, and when the bacilli localize them- 
selves by metastasis in any part, they produce lesions akin to those 
of pyemia. 

Because of the implication of the glandular system, especially the 
intrathoracic glands, it was assumed by many authors that infection 
in children is invariably accomplished by inhalation of the bacilli. 
The microérganisms are deposited in the lungs, and when attempting 
to invade the blood, they are retained by the lymphatic glands.!. When 
the localization of the lesion was found in the mesenteric glands, it was 
clear that ingestion of the bacilli was the channel of entry, and this was 
confirmed by the fact that in mesenteric tuberculosis bovine bacilli 
were often found. 

But we have seen that this is not necessarily the case. Entering 
via the digestive tract, the bacilli may reach the tracheobronchial 
glands with as much ease as when entering wa the respiratory tract. 
Behring and Calmette and their school maintain, in fact, that all 
tuberculosis, especially in children, is lymphogenous and hematogenous 
(see p. 54). 

From the facts presented in the chapters on Phthisiogenesis it is 
clear that tuberculosis during infancy and childhood is hematogenous, 
irrespective of the portals of entry of the bacilli. A study of the rates 
of mortality during the various ages of life confirms this view. As 
will be seen from the accompanying diagram (Fig. 90), pulmonary 
tuberculosis is a frequent cause of death in infants under two years 


1 See Allen K. Krause: Studies in Tuberculous Infection, Am. Rev. Tubercul., 1919, 
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PULMONARY TUBERCULOSIS IN CHILDREN 


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TUBERCULOSIS DURING INFANCY 449 


of age; between three and fourteen years of age comparatively few 
succumb to this form of the disease; only after fifteen years of age does 
it become very frequent and remains so until the age groups above 
eighty years. We know from clinical experience that when occurring 
during the first two years of life, pulmonary tuberculosis is almost 
invariably acute, and the chronic type is extremely rare at this 
age. On the other hand, all other forms of tuberculosis, including that 
of the glands, bones, joints, serous cavities, especially the meninges, 
and the intestines; in short, the hematogenous forms of tuberculosis, 
cause death most frequently during the first four years of life and are 
comparatively uncommon as a cause of death after the fifth year of 
life. 

It is thus clear that acute tuberculosis, as well as the hematogenous 
forms of this infection, have a different age incidence when compared 
with chronic phthisis, the disease which creates the main problem. 
Moreover, as was already shown, during the years when most of the 
human infections take place, between the second and the fourteenth, 
the mortality from all forms of tuberculosis is comparatively low; 
even hematogenous tuberculosis as a cause of death maintains the same 
rate throughout the rest of human life. It also shows that phthisis, 
which is a common cause of death in adults, is not necessarily preceded 
by infection with tubercle bacilli immediately before the disease manifests 
itself by symptoms. It shifts the problems of infection from the adult 
to the child. 


TUBERCULOSIS DURING INFANCY. 


We have shown that the child is born free from tuberculosis, and that 
infection, if it takes place at all, occurs post partum. Virchow, whose 
autopsy experience was as immense as that of any physician, stated that 
he never encountered a case of fetal tuberculosis. Infection in an infant 
is therefore invariably primary and almost always followed by symp- 
toms of disease. Indeed, as we have already shown, there are cases on 
record in which infants brought into contact with a consumptive for an 
hour or so developed tuberculous disease of a malignant type. When 
the infection is massive, acute general tuberculosis with implication of 
the glandular system, and often of the lungs, is almost invariably 
caused. 

The infant's organism behaves after a primary infection just as the 
very susceptible guinea-pig, the reason being that there is a primary 
infection of a body which has not yet been immunized by a previous 
mild infection. ‘These cases occur mostly in infants who live with 
tuberculous persons—the father, mother, sister, brother, or nurse being 
tuberculous and, in handling the infant, an opportunity is afforded to 
transmit the disease. Thus, Combe! found a family history of tuber- 
culosis in 90 per cent of his cases, if the word ‘‘family history” included 


1 Le Nourisson, 1916, 4, 1. 
29 


450 PULMONARY TUBERCULOSIS IN CHILDREN 


all persons who live in intimate contact with the family. Clinicians 
have found that in doubtful cases a careful family history is a great 
aid in diagnosis, provided it includes not only the father and the mother, 
but also brothers, sisters, servants and relatives and acquaintances 
who come to the house, and in contact with the infant. There is 
evidence tending to show that in some cases, though in less than is 
generally supposed, the infection is derived from bovine bacilli through 
milk from tuberculous cows. 





Fie. 91.—A primary cheesy focus the size of a lentil in a bronchus of the left lower 
lobe with miliary and conglomerate tubercles of the regional peripheral atelectatic lung. 
Caseation of the bronchopulmonary and lower tracheobronchial glands in the region 
of the right lower lobe. The glands on the left side are free. (Anton Ghon.) 


In many cases no exciting cause, except the source of infection, 
can be traced. In others some acute endemic disease of infancy is 
found to have produced a state of allergy. This is especially true of 
measles and whooping-cough, but any of the other contagious diseases 
of infancy may reduce the vitality and resisting powers of the infant, 
and infection is then followed by the characteristic acute form of 
tuberculosis. 


TUBERCULOSIS DURING INFANCY 451 


The period of incubation of tuberculosis in infants has not been 
exactly determined. In the few cases reported by Koch and Knipfel- 
macher! it appeared to be about seven weeks. Reuben? in New York 
found it to be from five to six weeks. 

Symptoms.—The symptoms depend on the mode of onset and on 
the parts of the body which bear the brunt of the infection. In those 
in whom tuberculosis follows in the wake of another disease, like 
whooping-cough, measles, etc., there are usually symptoms of broncho- 
pheumonia or meningitis, which carry off the patient within a few days 
or a week or two. In addition to the symptoms and signs of broncho- 
pneumonia, there are often found enlargement of the spleen and liver, 
and swelling of the superficial glands, the cervical, axillary, inguinal, 
ete. This form of acute tuberculosis is best seen in cases of tubercu- 
lous disease engendered by inoculation, as in infection of the wound 
after ritual circumcision. Arluck and Wincouroff,? and Holt’ have 
described such cases in detail. 

In those in whom the disease is slower in development, athrepsia is 
seen. It is noted that the child does not thrive despite the fact that its 
nourishment leaves little or nothing to be desired and the gastro- 
intestinal functions are fairly normal. There may be no fever at all. 
Still the emaciation proceeds frightfully. In some cases the emacia- 
tion consumes nearly all the subcutaneous adipose tissue and the thin, 
pale skin is stretched over the atrophied, softened, and bent bones. 
These infants usually have long hair on the back between the shoulder- 
blades and on the extremities; their eyes are sunken and the eyelashes 
are frequently long. In a large proportion, over 20 per cent according 
with T. C. Hempelmann, tuberculides are found on the body. — Finally 
the temperature begins to rise and may reach very high, and they 
succumb to symptoms of septicemia or meningitis. 

Examination of the chest may not show any changes, while in some 
we may find areas of defective resonance, bronchial breathing, or rales. 
In infants limited and circumscribed lesions are very difficult of locali- 
zation because we have no assistance on their part while exploring the 
chest. 

Cough may be absent altogether, but in some cases we meet with a 
peculiar cough caused by pressure of enlarged glands on the bronchi, 
or on the nerves passing through the chest. [Eustace Smith? first 
described this cough as spasmodic, occurring irregularly in paroxysms 
like those of pertussis, lasting only a short time and ending sometimes, 
though rarely, in a crowing inspiration. This cough has since been 
differently described by various authors. Schick® describes a respira- 
tory crow, or stridor, resembling the sound heard in asthma and in 


1 Ztschr. f. Kinderheilk., 1915, 13, 89. 

2 Arch. Pediat., 1916, 33, 171. 

3 Beitr. z. Klin. d. Tuberkulose, 1912, 22, 341. 

4 Jour. Am. Med. Assn., 1913, 61, 99. 

5 Wasting Diseases of Infants and Children, London, 1878. 
6 Verhandl. d. Ges. f. Kinderheilk., 1909, 26, 121, 


452 PULMONARY TUBERCULOSIS IN CHILDREN 


capillary bronchitis. It can, however, be distinguished from the latter 
by the fact that in asthma the cough is paroxysmal while the stridor 
in bronchial adenopathy in infancy is continuous, lasting without 
change for weeks and months. The French have described it as towa 
coqueluchoide, and Striker compares it with the bark of a hoarse puppy. 

In many cases dyspnea is observed. It may be inspiratory or expira- 
tory, though in infants it is most commonly expiratory. It is best 
differentiated from dyspnea due to trouble in the larynx by the fact 
that in adenopathy the voice remains clear. With the growth of the 
glands, the dyspnea increases in intensity and in extreme instances 
asphyxia occurs as a result of occlusion of a bronchus, either suddenly 
or slowly. In these cases cyanosis of the extremities, face, etc., is 
marked, and inspiratory retraction of the lower parts of the chest, is a 
striking sign, ete. Many of these succumb to pulmonary edema. 

In most of these slow cases the cachexia progresses until finally 
the child succumbs to some intercurrent disease or to tuberculous 
bronchopneumonia. In rare instances a softened gland ruptures 
into a bronchus causing aspiration pneumonia. A relatively large 
proportion end with tuberculous meningitis. Investigations made 
by the writer! of children under six years of age living in a tuberculous 
milieu in New York City have shown that 16 per cent succumb to 
meningitis, as against only 2.6 per cent among the general population. 

Other infants may be anemic and underfed for months. They do 
not thrive in spite of all efforts to improve their nutrition. Finally, 
the marasmus assumes an acute character, the fever rises and they 
succumb to exhaustion or more commonly to some intercurrent disease. 

Diagnosis.—It is clear that the diagnosis of tuberculosis in infancy 
is not an easy matter. Hamburger’s? advice should be followed by 
all who have infants under their care: Think of tuberculosis in every 
case in which no other diagnosis can be made. This dictum is shared by 
nearly all other pediatrists who have given thought to the problem. 
Tubercle bacilli cannot be discovered because infants do not expec- 
torate. Holt has, however, often found them by swabbing the throat 
with a pledget of cotton. A positive tuberculin (von Pirquet) reaction 
in an infant under one year is sufficient to clinch the diagnosis. Un- 
fortunately during the course of measles or whooping-cough, and in 
tuberculous meningitis, the tuberculin reaction is apt to be negative, 
despite the presence of tuberculous infection. 

Prognosis. —'he prognosis of tuberculosis in infancy is very gloomy. 
In fact, it may be stated that the younger the infant the more unfav- 
orable the prognosis. During the first three months of life hardly 
any survive infection; the vast majority of those infected during the 
second three months of life succumb to the disease or to some inter- 
current infection; the outlook for infants between six and eighteen 
months is very unfavorable when infected with tuberculosis. Infants 


1 Arch. Pediat., 1914, 31, 197. 
2 Brauer, Schréder, and Blumenfeld’s Handbuch d, Tuberkulose, Leipzig, 1915, 5, 6. 


TUBERCULOSIS DURING EARLY CHILDHOOD 453 


infected by tuberculous mothers succumb earlier than those infected 
by their fathers or others. Herbert Koch! suggests that the reason is 
probably that mothers infect their infants much earlier than fathers. 

It appears to be the consensus of opinion of most pediatrists that all 
tubercles during the first two or three years of life are active, that the 
lungs show no tendency to limitation of the disease, and that there are 
no reparative processes to be noted when examining the lungs of 
infants who succumbed to tuberculosis. No cicatrization or calci- 
fication is to be observed. 

The corollary has been drawn that all infants showing signs of 
infection with tubercle bacilli—a positive von Pirquet reaction—are 
doomed. The writer cannot agree with this. We have followed 
infants showing positive von Pirquet reactions during the first three 
months of life growing into healthy children. It appears that the 
dangers of developing active tuberculous disease and the acuteness of 
the process engendered are in inverse ratio to the age at which the infection 
takes place. The younger the infant the more unfavorable the prognosis. 
But even among very young infants cicatrization and calcification of 
the lesion may occur. In another place I have collected evidence 
showing that such healed lesions were found at autopsies made on 
infants who died from other causes. ‘The writer has observed numer- 
ous infants living with their tuberculous parents become infected with 
tuberculosis, yet they grew into healthy children. Some have been 
followed for more than ten years. Mark S. Reuben in New York had 
under his care from 1909 to 1916, for shorter or longer periods, 23 
infants who gave a positive tuberculin reaction. Nine of the 23 
infants who became infected during their first year of life kept up in 
good health for from one to five years. ‘I’. C. Hempelmann studied the 
fate of 130 infants under two years of age with pulmonary tuberculosis. 
He found that the mortality among the infants under one year of age 
was 78.7 per cent; from one to two years of age, 57.4 per cent; and for 
the two years, 68 per cent. 

It is thus clear that while tuberculous infection during infancy is 
very serious, it is by no means hopeless, as some writers have stated. 
At least one out of three survives. 





TUBERCULOSIS DURING EARLY CHILDHOOD. 


Significance of Tuberculosis during Childhocd.—In our study of the 
epidemiology of tuberculosis we have seen that the child is born free 
from tuberculosis, but that sooner or later, coming into contact with 
tuberculous individuals, or their discharges, or consuming milk from 
tuberculous animals, it is infected with tubercle bacilli. We have 
also shown that during the first year of life relatively few—between 
5 and 10 per cent—are infected with tubercle bacilli. During the 





1 Ergebn. d. inn. Med. und Kinderheilk., 1915, 14, 99. 


454 PULMONARY TUBERCULOSIS IN CHILDREN 


second year more are infected, and the number of infections keeps on 
growing so that at the age of fifteen over 90 per cent show unmistak- 
able signs of harboring tubercle bacilli in the body. A study of the 
mortality from tuberculosis according to age groups has shown that 
the mortality from this disease is very high during the first two years 
of life. Considering the malignant clinical forms of the disease which 
have been described above, the reason is clear. But beginning with 
the third year the number that succumbs to this disease is very small - 
and this low mortality keeps on until the fifteenth year, when there is 
another increase which keeps on rising, so that from the twentieth 
year onward the maximum has been reached, which keeps up until far- 
advanced age. 

It is thus clear that during the years when most infections with tubercle 
bacilli take place, the mortality vs at its lowest. It is also clear that if 
infection is to take place, which we have shown to be inevitable for 
those living in large industrial towns and coming into contact with 
many people, it is best that it should occur during childhood. Appar- 
ently, during this age period death due to tuberculosis is exceptional. 
This point will be discussed again when speaking of the prophylaxis 
of tuberculosis. 

Infection and Morbidity. We must again emphasize the difference 
between infection with tubercle bacilli, and disease due to this micro- 
organism. It appears that the vast majority of children infected with 
tubercle bacilli do not show any clinical manifestations of disease, other- 
wise over 50 per cent of children in large cities would be sick and 
in need of careful treatment; at the age of ten over 75 per cent would 
be sick and in need of dietetic, specific, institutional, or climatic treat- 
ment. Scientific tests prove conclusively that the vast majority of 
children have been infected, and but few show clinical manifestations 
of disease; hence the bulk of infections at that age cause no disease, 
and may be disregarded by the clinician. Some, however, do show 
clinical manifestations of disease. 

Tuberculous Adenopathy.—Scrofula.—A frequent manifestation of 
tuberculosis in children is enlargement of the glands, popularly known 
by the ancient and venerable name scrofula. Most commonly the 
cervical glands are affected, those below the angle of the lower jaw, 
or in front of the sternocleidomastoid muscle, and, in some, in the 
supraclavicular fossee, become enlarged and hard. They may be so 
small as to be hardly palpable, but in others they become visible, and, 
in extreme cases, two chains of enlarged glands are seen on both sides 
of the neck, adherent to one another and to the skin. Later they may 
soften, rupture spontaneously, discharging pus, and leaving fistule 
which heal with difficulty, the remaining scars being ugly and dis- 
figuring. 

In some cases tuberculous lesions of bones develop, especially of the 
small bones of the carpus, tarsus, and phalanges; the epiphyses of the 
long bones are only rarely implicated. The common forms of these 


TUBERCULOSIS DURING EARLY CHILDHOOD 455 


osseous lesions are spina ventosa and tuberculous dactylitis, usually 
affecting the metacarpal bones and phalanges of the hands. The finger 
then is enlarged, bulbous, in characteristic fusiform shape, but slightly 
tender. In some instances the inflammatory induration is absorbed 
later, but more frequently softening and necrosis of the bone takes 
place, and sequestra are discharged, leaving ugly sinuses which heal 
sluggishly, and finally leaving more or less crippled fingers. 

The tuberculous character of scrofulous lesions has been debated, 
but the consensus of opinion at present seems to favor the tubercle 
bacillusas the etiological agent. Cornet considers scrofula a product of 
mixed infection with pyogenic and tuberculous organisms, but the 
weight of recent opinion appears to be in favor of its being specific, 
and that no other organism outside the tubercle bacillus need be 
concerned in its etiology. Its relation to tuberculosis in later life 
has recently been discerned. Bartel and Eschrich have shown that 





Fig. 92.—Multiple spina ventosa. (Tibler.) 


scrofula is a form of infantile tuberculosis which occurs only in subjects 
possessing the lymphatic diathesis. In a recent study of the subject 
F. Spieler! arrives at the conclusion that the main channel of infection 
is the skin in which repeated inoculations of small numbers of tubercle 
bacilli takes place, and also the mucous membranes of the nose, throat 
and mouth. It is well known that children with the lymphatic con- 
stitution display strong tendencies to catarrhal conditions of the 
accessible mucous membranes. Scrofula may thus be looked upon as 
a manifestation of the defence reaction of the lymphatic child against a 
superimposed tuberculous infection. The lymphatic constitution is 
the preliminary condition in the clinical picture of scrofula; it is the 
primary, or predisposing cause. When in such a child tuberculous 
infection takes place, the glandular manifestations of the disease 


result. 
1 Skrofulose und Tuberkulose, Leipzig, 1920. 


456 PULMONARY TUBERCULOSIS IN CHILDREN 


The relations of scrofula to pulmonary tuberculosis are rather 
interesting, and not appreciated to the extent they deserve. As will 
be shown later on (see Chapter XXX), it appears that scrofulous 
children only rarely develop pulmonary tuberculosis in later life, and 
when a lung lesion does occur, it runs a very mild course and tends to 
cicatrization, a fact which was already observed by clinicians several 
generations ago. 





Fia. 93.—Tuberculosis of cervical and axillary lymph nodes in an eight-year-old boy. 
(Carr.) 


On the whole, the prognosis of scrofula is very good, though the 
patient may ultimately remain with ugly and disfiguring scars on the 
neck. But these children are very susceptible to the acute endemic 
infectious diseases, and when attacked by them, especially by measles, 
whooping-cough, diphtheria, etc., the prognosis is serious. Escaping 
the ravages of these acute infections, they usually grow into healthy 


TUBERCULOSIS DURING EARLY CHILDHOOD 457 


men and women, and are less likely to succumb to pulmonary tuber- 
culosis than others, as will be shown in another chapter of this book. 

Not all enlarged glands observed in children are scrofulous, or tuber- 
culous, in origin. Moreover, in most of the children having enlarged 
glands, even of tuberculous origin, the symptoms are negligible, or there 
are no other clinical manifestations at all. Thus, we often discover 
enlarged glands on the neck, or within the thorax, of children who are 
in excellent condition of health. In some we find the glands enlarged 
for some time, then there is a recession, the swellings go down or dis- 
appear, while the children had kept up their activities at school, and 
were none the worse for their experience. In others, the appearance 
of the glands is concurrent with the occurrence of some disease, 
like measles, scarlet fever, whooping- 
cough, ete.; they remain enlarged 
during convalescence, but after 
complete recovery they recede, or 
disappear permanently, or may re- 
turn when some other exciting cause 
is again operative. We may thus 
see in many children a tendency to 
enlargement of the glands whenever 
an exciting cause is operative, but 
the innate forces of resistance are at 
work, and recovery takes place in a 
short time, spontaneously, or after 
some treatment has been instituted. 

If we should take enlarged cervi- 
cal glands as an invariable indication 
of active tuberculous disease in chil- ‘ 
dren, we would find very few raised y 
under adverseeconomic and hygienic set Hl 
conditions who are free from this Fig. 94.—Tuberculosis of the sub- 
disease. Thus, among 692 children maxillary glands. 
of tuberculous parentage examined 
by the author, 469, or 67.8 per cent, had swollen cervical glands. A 
careful examination of children attending dispensaries shows that 
between 50 and 75 per cent have palpable cervical glands. Most of 
them are due to carious teeth, hypertrophied tonsils and adenoids, 
stomatitis, eczema or pediculi of the scalp, ete. Correction of these 
conditions is usually effective in reducing the size of the glands. At 
any rate they are as a rule not tuberculous. 

Symptoms of Glandular Tuberculosis in Children.—The appearance 
of glandular tuberculosis is accompanied, often preceded, by symptoms 
which are troublesome, and need careful study for their recognition. 

Of these symptoms the following are the most important: Emacia- 
tion, fever, nightsweats, anemia, anorexia, etc. 














458 PULMONARY TUBERCULOSIS IN CHILDREN 


Emaciation.—A healthy child gains in weight constantly, and if it 
is regularly weighed, say every month, it will be found that the scale 
registers more than at the preceding weighing. While in normal 
adults a lack in this direction is not necessarily an indication of disease, 
because they may have reached their normal standard, or even exceeded 
it, with children conditions are different. Commensurate with their 
gain in height, there must be a gain in weight in children of school 
age. It is known as the normal increment in the size of the body. 
When a child does not gain in weight it is, with few exceptions, an 
indication of disease. 

To ascertain this gain in weight, various tables have been prepared 
by anthropometrists, and reproduced in many text-books on pediatrics. 
But I want to warn the practitioner against comparing the weight of 
a child under his care with that given in any of these tables. To begin 
with, the weight given in the table for each age is an average of a large 
number of children, and averages permit variations that are normal. 
The normal weight of the child depends solely on its height, and there 
are perfectly healthy children and adults who are short of stature. 

What the physician should look for is a steady gain. If this is not 
found, it is clear that the child is sick. At any rate, it demands an 
explanation. In many cases it may be due to some intercurrent 
non-tuberculous disease. But it should be found and treated. When 
we find that a child is not gaining in weight for several months, it is 
equivalent to a steady loss in an adult. If there is no morbid condition 
to account for it, tuberculosis may safely be suspected as the cause. 
A careful physical examination will, in many cases, reveal enlarged 
intrathoracic glands. 

An exception is to be mentioned. Infants may be suffering as a 
result of tuberculous infection and show no signs of emaciation for 
along time. This is evident from the fact that tuberculous menin- 
gitis, or bronchopneumonia, often attacks well-nourished infants. In- 
fantile tuberculosis, unless the gastro-intestinal tract is affected, does 
not always lead to cachexia. 

With the emaciation there is often to be observed anemia, mani- 
festing itself in marked pallor of the skin and mucous membranes, 
though an examination of the blood may not disclose any definite 
changes in its cytology. 

Fever.— Whenever tuberculous glands cause trouble there is a rise in 
temperature. Hamburger’s conception of tuberculous disease supplies 
the theoretical basis for the fever in these cases. He looks upon all 
clinical exacerbations of tuberculosis as spontaneous tuberculin reac- 
tions due to a sudden flooding of the body juices with tuberculin, 
producing the same symptoms as we produce artificially by injecting 
tuberculin. In other words, the fever is a manifestation of auto- 
inoculation. 

The healthy child’s temperature oscillates between 98.8° and 99.8° 
I’. Whenever it rises above these limits, it is to be considered patho- 


TUBERCULOSIS DURING EARLY CHILDHOOD 459 


logical, and an explanation is to be sought. If no cause can be found 
for elevation of temperature, which is observed persistently for several 
weeks, tuberculosis is to be thought of. In most cases it will be found 
that, in addition to the thermometrical findings, there are also symp- 
toms of hyperthermia, such as anorexia, languor, etc. The child may 
feel refreshed and lively during the morning hours, but late in the 
afternoon it is flushed, tired, and seeks rest. 

In evaluating thermometrical findings it must always be remem- 
bered that the fluctuations in the temperature are much more pro- 
nounced in children than in adults. Thus E. Wynn! found that among 
1000 children 261 had temperatures of 99° F. or over, and of these, 
112 presented no obvious pathological condition to account for the 
hyperthermia. Mary E. Williams? found among 1000 school children 
between the ages of twelve and fourteen years that no less than 55.5 
per cent had temperatures of 99.6° F. and higher. 

There are two reasons to account for the oscillations of the tem- 
perature in children. The heat regulating mechanism is more apt to 
be disturbed by slight factors than in adults, as is shown by the fact 
that nearly all pathological conditions produce higher fever in them 
thaninadults. Then, there are so many subacute or chronic conditions 
which produce mild fever in children, that it would be wrong to base a 
diagnosis of tuberculosis on thermometrical findings alone. But when 
the temperature is found elevated persistently for several weeks in a 
child, and other symptoms of tuberculosis are present, while no other 
cause can be discovered, the patient is to be kept under careful observa- 
tion. A difference of more than 1.5° F. between the minimum and 
maximum temperature of the day, when persistent, points to tuber- 
culosis, when no other cause can be found. 

Nightsweats.—As a symptom of tuberculosis in children night- 
sweats have not the same significance as in adults. Many non-tuber- 
culous children sweat during the night. In a study of the physiological 
phenomena of sleep in children, Czerny* found that the intensity of 
evaporation from the skin goes hand-in-hand with the depth of the 
sleep. At the time when sleep is most intense, at its maximum, the 
skin is warm and moist, and usually profuse perspiration on the face is 
noted. ‘This is not to be considered pathological. 

To be of diagnostic significance, nightsweats in children must appear 
during the second half of the night and be so profuse as to soak through 
the bedclothes. ven in such cases they may not be pathognomonic 
of tuberculosis; the possibility must always be borne in mind that 
they may be of nervous origin, especially in older children. At any 
rate, nightsweats are often absent in tracheobronchial adenopathy, 
though with each exacerbation of the symptoms of activity they are 
to be observed. 


1 Public Health, 1913, 26, 136. 
2 Lancet, 1912, 1, 1192. 
3 Jahrb. f. Kinderheilk., 1892, 33, 22. 


460 PULMONARY TUBERCULOSIS IN CHILDREN 


In tuberculous bronchopneumonia in children nightsweats are the 
rule, but in non-tuberculous cases they are often a prominent and 
annoying symptom. 

Cough. —Cough is another symptom of active tuberculosis in children. 
It is non-productive, unless the sputum is derived from the naso- 





Fie. 95.—Diagram showing greater number of glands located on the right side. 


pharynx, which is not uncommon. Hamburger says that it is never 
absent in active, incipient cases, and when cough lasts more than a 
week the possibility of tuberculosis should be considered and a thorough 
search for other symptoms and signs of the disease should be inaugu- 
rated. In advanced stages of the disease cough may be lacking, espe- 
cially when there is an arrest in the progress of the disease, which is not 


TUBERCULOSIS DURING EARLY CHILDHOOD 461 


infrequently the case in children between eight and fourteen years of 
age. But even in these cases we meet with frequent exacerbations of 
the disease when the child coughs more or less. 

We must, however, emphasize that in children over three years of 
age cough is only of significance as a symptom of active tuberculosis 
when other symptoms are present, especially emaciation. When 
a child thrives, despite a chronic cough, it will be found that there is 
another cause, especially chronic or subacute catarrh of the nose and 
throat, particularly during the winter months. These children also 
may have enlarged cervical glands, which are neither tuberculous, 
nor scrofulous. In fact tuberculosis 1s rare in children with hyper- 
trophy of the lymphovd tissues of the rhinopharynx. Asthma also is often 
a cause, and so is chronic bronchitis of the upper lobe, though we 
must be careful when finding unilateral bronchitis, which is almost 
invariably tuberculous. Signs of bronchitis of the lower lobe, even if 
unilateral, point to bronchiectasis and hardly ever to tuberculosis. 
Bronchiectasis is very common in children. 

The paroxysmal and the brassy cough, as well as the expiratory 
stridor of infants, have already been described. 

Children presenting any or all of these symptoms—emaciation, 
fever, nightsweats, cough, ete.—require a careful physical examination, 
and if these symptoms are due to active tuberculosis, we almost invari- 
ably find local tuberculous changes—that the glands are affected 
except in those over eight years of age, among whom localized pulmo- 
nary tuberculosis of the same character as in adults may be found. 

In many cases we note that despite the fact that the physical devel- 
opment of the child is decidedly inferior, its mental capacities are 
above the average. ‘These children are often precocious, exceptionally 
good pupils at school, and if with artistic inclinations, they may be 
excellent musicians, etc. On the other hand, in quite a large pro- 
portion of cases the smouldering tuberculous process has quite the 
opposite effect—the child is backward in his studies, lazy and listless. 

Physical Signs of Tracheobronchial Adenopathy.—The best that 
‘an be said about the physical diagnosis of tracheobronchial adenopathy 
is, that it is very indefinite; at any rate, all the criteria taken for 
proof of the existence of enlarged glands within the thoracic cavity do 
not enlighten us whether the process is active, and demands active 
treatment, or is merely an innocuous enlargement of the glands of no 
clinical importance, as it actually is in the vast majority of cases. 
Judging by the anatomical relations of these glands, it is clear that they 
must attain some size before they become discoverable by percussion 
and auscultation of the chest. But that they often do attain large 
dimensions may be assumed when we consider the size attained by the 
cervical glands at times. It may be said that there seems to be a rela- 
tion between the size of the glands and the effects they produce. For 
this reason tracheobronchial adenopathy may be more easily diagnosed 
in infants in whom these glands are naturally large, than in children in 
whom they are comparatively small, 





462 PULMONARY TUBERCULOSIS IN CHILDREN 





Fias. 96 and 97.—Composite drawings showing the relationship of the bronchial 
glands to the thoracic wall in the adult. The glands are according to Sukiennikow, and 
the trachea and bronchi are after Blake (Am. Jour. Med. Sci., 1899, 117, 320). In the 
child the trachea bifurcates at about the level of the intervertebral disk between the 
fourth and fifth thoracic vertebree, which corresponds nearly to the tip of the fourth 
thoracic spine. This is about opposite the articulation of the third costal cartilage 
anteriorly, (Stoll,) 


TUBERCULOSIS DURING EARLY CHILDHOOD 463 


This group of glands includes those located around the trachea and 
bronchi, mainly in front of the bifurcation of the trachea. Pathologi- 
cally, it has been found that those around the right bronchus are more 
liable to attain very large dimensions and produce symptomsand signs of 
the disease. From the practical standpoint, in addition to the anterior 
and posterior mediastinal glands, there are three groups which may 
become swollen because of tuberculous infection: At the bifurcation 
of the trachea we have the tracheobronchial lymph nodes; along the 
main bronchi there are the bronchial lymph nodes; and at the hilus 
of the lungs there are the pulmonary lymph nodes, which also surround 
the bronchi, and communicate through lymph spaces with the paren- 
chyma. In fact, all these glands receive their lymph from the pul- 
monary tissue and the bronchi. Considering their anatomical rela- 
tions it is clear that when enlarged, they may exert pressure upon 
the bronchi and trachea, as well as on the nerves and bloodvessels 
passing through the chest. ‘They may produce symptoms because of 
pressure exerted on the vagus and recurrent laryngeal nerves and the 
superior vena cava. ‘They may even press upon the phrenic nerve, 
the arch of the aorta, innominate veins, ete. But this is exceptional 
despite the fact that text-books give so many signs revealing pressure 
on the various structures. The anatomical relations of these glands 
are shown vividly in the illustrations (Figs. 96 and 97, page 462) from 
Stoll,! based on Sukiennikow’s? anatomical researches. 

Inspection.—On inspection the thorax is often found deformed in 
those who have had enlarged glands; indeed, some of the deformities 
produced by the intrathoracic glands are difficult to differentiate from 
the changes produced by early rickets. In some cases we find the 
typical phthisical thorax, the habitus phthisicus—a long, narrow chest 
with the ribs slanting downward at an acute angle, and narrow inter- 
costal spaces. Children with such chests have passed through several 
attacks of glandular enlargement and may, at the time of examination, 
be in fair health. In many we see what Stoll calls the “hilus dimple.” 
If the breath is held at the end of inspiration there is seen an apparent 
retraction on one or both sides in the second interspace. Owing to 
lack of expansion of one apex, the chest wall lags with inspiration. 
In old cases this “dimple” may remain permanently, owing to pleural 
adhesions or cicatrization of the peribronchial tissues at the hilus 
(Figs. 98 and 99). 

This phthisical chest, which some authors consider predisposing to 
phthisis, 1s in fact proof that the patient has been tuberculous for a 
long time, and in children it is proof that the thoracic glands have 
been enlarged. In our investigations of the form of the chest in 
children of tuberculous parentage, we found that at birth the chest is 
almost invariably normal, and only when tubercles affect the intra- 


1 Am. Jour. Med. Sci., 1911, 141, 83; Ibid., 1914, 148, 369; Am. Jour. Dis. Children, 
1912, 4, 333. 
2 Berl. klin. Wehnschr., 1905, 11, 316, 347, 369, 


464 PULMONARY TUBERCULOSIS IN CHILDREN 


thoracic viscera are changes in its form produced. In some cases 
unilateral bulging of the chest wall is noted, especially the first two 
interspaces near the sternum. 

Enlarged veins are often visible on a chest containing enlarged 
glands. ‘They are usually seen on the upper part of the thorax, mostly 
bilateral though not symmetrical, and at times unilateral. In my own 
cases, 37.5 per cent of children with tracheobronchial adenopathy had 
enlarged and visible veins on the thorax, and of these, three-fourths 
were unilateral. Of those in whom the diagnosis of latent tuberculosis 
was justified, or in whom it was strongly suspected, 25 per cent showed 
this sign, while among the manifestly healthy only about 1 per cent 
had enlarged veins on the thorax. Stoll found enlarged and visible 
veins on the thorax in 92 out of 173 cases; of these 50 per cent were 
tuberculous. 





Fia. 98 TI'ie. 99 
Fies. 98 and 99.—The “‘hilus dimpie.” (Stoll.) 


It thus appears that this is a fair sign of compression of the main 
trunks of the intrathoracic veins by enlarged glands or adherent 
pleura. My general experience, however, urges me against hasty 
diagnosis based on this sign alone. It is met with in many healthy 
children, especially such as have a delicate and transparent skin, and 
also in anemia. In adults, it is often seen in women during lactation, 
when it may be unilateral, and in persons suffering from non-tuber- 
culous affections of the bronchi, lungs, and pleura, especially chronic 
bronchitis, asthma, and pulmonary emphysema (see p. 301), 


TUBERCULOSIS DURING EARLY CHILDHOOD 465 


Percussion.—A great deal has been written about percussion as an 
aid to the diagnosis of tracheobronchial adenopathy. But as a matter 
of fact there are many children with undoubted enlargement of these 
glands in whom the percussion note elicited over every part of the chest 
is practically normal. When we consider the topographical position 
ot the bifurcation of the trachea, it is clear that the glands must become 
very large to produce dulness anteriorly or posteriorly over the surface 
of the chest. ‘The various spécial methods like Koranyi’s! vertebral 
percussion, which has been elaborated in this country by John C, 
Da Costa,? do not give satisfaction. In many cases, however, there is 
found paravertebral dulness on light percussion. ‘The areas that may 
be found affected correspond to the hilus—the interscapular space, 
especially the right, and anteriorly in the upper two interspaces 
near the sternum. ‘To elicit this, very light percussion is necessary 
because of the thinness and resilience of the thoracic walls in the child. 
It may be found when the glands are not very much enlarged; then it 
is due to the engorgement of the bloodvessels and lymphatics which 
exists in the region of the hilus during the course of certain acute 
infectious diseases. It is the collateral inflammation described by 
Tendeloo.* 

This defective resonance is only rarely bilateral. Anteriorly it must 
be differentiated from the dulness due to an enlarged thymus. The 
latter is usually beneath the sternum, while in bronchial adenopathy 
the dulness is mainly at the side of that bone, mostly to the right. 
We must mention that there is normally an oval area of dulness 
between the first and fifth thoracic vertebra, extending an inch or 
two outward on each side of the spine, to which William Ewart! 
has called attention. But in cases of glandular enlargement it is usually 
unilateral—one interscapular space is dull. I have seen a few cases in 
which enlarged thoracic glands produced dulness all over one side ot 
the chest. It may be taken as an indication of compression of the 
main bronchus by the enlarged glands. Another point is that this 
dulness, to be indicative of adenopathy, must be permanent, found 
during several examinations. As has been pointed out by Grancher 
and J. E. H. Sawyer,’ in debilitated and rachitic children there are 
observed transient areas of dulness, due to a bronchus being plugged 
with secretions and the resulting atelectasis of the air vesicles it 
supplies. 

Auscultation.—In my experience auscultation has been of more 
service in attempting to diagnosticate intrathoracic glands. Nor- 
mally the breath sounds in children are louder and somewhat harsher 
than in adults—puerile. But this, in healthy children, is heard all 


1 Ztschr. f. klin. Med., 1906, 60, 295 

2 Am. Jour. Med. Sci., 1909, 138, 815; 1913, 146, 660. 
3 Sixth Intern. Congr. on Tuberculosis, 1908, 6, 197. 
4 British Med. Jour., 1912, 2, 966. 

5 Birmingham Med. Review, 1912, 19, 57. 


30 


466 PULMONARY TUBERCULOSIS IN CHILDREN 


over the chest. Swollen glands alter them in circumscribed areas. 
Thus, when large, we may find feeble breathing over a limited area, 
owing to compression of a bronchus, or to modifications in the pulmo- 
nary circulation in that region. In rare instances the breath sounds are 
feeble over a lobe, or an entire lung, anteriorly and posteriorly, which 
also is due to compression of the supplying bronchus. But this is 
hable to great variations. I have followed some children for years 
and found that at times there are modifications in the breath sounds in 
a given area which shift so that at the next examination, one or more 
months later, the modification is found at another place. It may be 
found that during an attack of an intercurrent disease, rhinopharyn- 
gitis, influenza, or any of the exanthemata, etc.—when the glands 
swell up and there is an exacerbation of the tuberculous process—the 
auscultatory phenomena make their appearance to disappear after the 
acute process is gone. 

Anteriorly the auscultatory signs in children are uncertain, because 
normally we may hear the tracheal sound at the sides of the manu- 
brium in emaciated, but non-tuberculous, children with narrow chests. 
Still, when tubular breathing is heard unilaterally at the side of the 
sternum it speaks for enlarged glands. Posteriorly, bronchial or harsh 
vesicular breathing in the interscapular space of one side is an indica- 
tion of the transmission of the tracheal murmur by enlarged glands 
which act as sound conductors. In mild cases only prolonged expira- 
tion is heard in one interscapular space, but in those in which the glands 
are very much enlarged, the breathing over a limited area may be 
tubular, or exquisitely bronchial; almost the same as is audible when 
listening directly over the trachea. 

D’Espine’s Sign: Tracheophony.— About thirty years ago A. d’Espine! 
described a sign of enlarged tracheal glands which appears to be more 
satisfactory than any other symptom or sign at our command at 
present. It consists in auscultation of the voice, especially the whis- 
pered voice, along the course of the trachea posteriorly. He described 
this sign as follows: The patient is told to count “one, two, three,” 
or “thirty-three,” as clearly as possible (younger children may be 
told to say “papa,” ““mamma’’) while the examiner auscultates with 
the naked ear, or better with a stethoscope, the spines of the cervical 
vertebrae. So long as we listen to the cervical spines, we hear the 
characteristic tracheal tone and each word is quite clear. In a normal 
child this clear voice stops abruptly as soon as we reach the seventh 
cervical spine where the lung begins; but in cases with bronchial 
adenitis the clearness of the voice; or the tracheal tone, continues 
lower down, from the first to the fifth thoracic vertebra. It is at this 
spot that the main localization of the enlarged bronchial glands is 
found. The transmission of the tracheal tone in these cases is effected 
by the enlarged glands which surround the trachea at its bifurcation 


1 Traité des Malad. de l’enfance, Paris, 1900, p. 856. 


TUBERCULOSIS DURING EARLY CHILDHOOD 467 


and often reach the spinal column, acting as sound conductors between 
the trachea and spine. 

When auscultation of the full voice gives uncertain results, the 
patient is told to whisper “thirty-three,” which is even more reliable 
than the bronchophony just spoken of. It must always be borne in 
mind that in healthy children and adults, bronchophony and the 
whispered voice stop abruptly at the seventh cervical spine, and when 
heard lower it is a sure sign of something interposing between the 
trachea and the spine, and acting as a voice conductor. 

This sign of tracheobronchial adenopathy has been extensively 
tried in France and many report that it is more reliable than any 
other sign. Barot! found it superior to percussion, and even more 
trustworthy than roentgenography for the purpose of ascertaining the 
presence or absence of enlarged thoracic glands. In this country it 
has been strongly recommended by Stoll, Sewall,? Howell,’ Honeij,‘ 
and others. 

In evaluating this sign it must be borne in mind that the height 
of the bifurcation of the trachea, where the glands are most likely 
to become enlarged in tuberculosis, differs according to the age of the 
patient. In infants and young children it is on a level with the seventh 
cervical vertebra. But with advancing age it sinks lower and lower. 
At the age of eight it reaches the second or third thoracic vertebra, and 
at twelve it is found as low as the fourth. In adults, especially in 
senile individuals, it may be found as low as the fifth or sixth thoracic 
vertebra. Therefore, ina child of ten, the transmission of the whispered 
voice to the third thoracic vertebra may not mean enlarged glands in 
the chest. 

It must also be emphasized that the mere transmission of the vocal 
resonance as heard over normal lungs is not d’Espine’s sign. ‘This is 
found very often in children without enlarged glands. It is the trans- 
mission of the characteristic tracheal timbre which counts. In most 
cases it is heard not only along the spine, but also in the interscapular 
space on one side; at times bilaterally. 

I have tested this sign in various ways and found it most satisfac- 
tory. In several cases the roentgenographic plate failed to disclose 
the presence of enlarged glands while d’Espine’s sign revealed them. 

Smith’s Sign.—Eustace Smith’s sign of bronchial adenopathy 
remains to be mentioned. It consists in this: If the child be made 
to bend back the head, so that the face becomes almost horizontal, 
and the eyes look straight upward at the ceiling above him, a venous 
hum, varying in intensity according to the size and position of the 
diseased glands, is heard with the stethoscope placed upon the upper 
bone of the sternum. As the chin is now slowly depressed, the hum 
becomes less loudly audible and ceases shortly before the head reaches 


1 Arch. médicales d’Angers, 1907, 12, 18. 
2 Jour. Am. Med. Assn., 1913, 60, 2027. 3 Am. Jour. Dis. Children, 1915, 10, 90. 
4 Jour. Am. Med. Assn., 1913, 57, 958. 


468 PULMONARY TUBERCULOSIS IN CHILDREN 


its ordinary position. Smith explains this phenomenon in this fashion: 
While the head is bending backward, the lower end of the trachea is 
tilted forward, carrying with it the glands lying in its bifureation, and 
the left innominate vein, as it passes behind the first bone of the 
sternum, is compressed between the enlarged glands and the bone. 

In my own experience this sign is not very reliable. It is found in 
short-necked children without enlarged glands, and is absent in many 
with adenopathy. Gibson! pointed out that it is mostly found in 
children who have enlarged veins in the neck and on the chest. 

Reflex Symptoms.— There are other symptoms of tracheobronchial 
adenopathy which are described in great detail in text-books, but 
which are, in fact, very rare and may be left out of consideration in the 
average case. ‘Thus, pressure on the recurrent nerve may produce 
paralysis of the right vocal cord; pressure on the sympathetic may 
produce differences in the size of the pupils. Pressure on the vagus 
may produce tachycardia and palpitation, transient or permanent. 
But these symptoms are very rare and are not conclusive even when 
encountered. 

In younger children caseated glands may break through into adjoin- 
ing structures, the bronchi, trachea, esophagus, etc. More rarely 
yet, the swollen glands acquire such dimensions that by pressure on 
a bronchus they prevent the entry of air into the part of the lung 
supplied by this tube; or by pressure on the trachea fatal asphyxia is 
produced. ‘There have even been reported cases of rupture of a gland 
into the aorta. But these cases are extremely rare and may be con- 
sidered medical curiosities. 

Roentgenography.— With the enthusiasm of the first years of roent- 
genography, we thought that with the aid of the x-rays we had at last 
found a means for positively identitying enlarged tracheobronchial 
glands. Roentgenographers often made diagnoses of tuberculosis in 
children who showed no symptoms of active disease, and continued well 
indefinitely. 

This was but natural, considering that normal glands allow the 
rays to pass through without casting any shadows, unless there is 
engorgement. Caseated glands cast a shadow which is occasionally 
distinct, but at times very indefinite. Only calcified glands cast a dis- 
tinct shadow which may be identified in the vast majority of cases. But 
calcified glands, tuberculous in origin undoubtedly, are an indication 
that the disease has come to a standstill; in fact, this is the only mode 
of cure of caseated glands. 

Under the circumstances the most easily diagnosticated cases of 
tracheobronchial adenitis, when the x-rays are used for the purpose, 
are those which have no significance clinically—those with calcified 
glands. When we attempt to clear up a case in which the glands are 
swollen, but neither caseated nor calcified—in other words, at a time 


‘1 British Med. Jour., 1906, 2, 1051. 


TUBERCULOSIS DURING EARLY CHILDHOOD 469 


when therapeutic measures may be inaugurated with a good chance 
of helping the patient—the x-rays very frequently fail to give conclusive 
proofs of the existence of trouble. On the other hand, they show old 
-and calcified glands which may not be, and often are not, the cause 
of the clinical symptoms for which the patient consults us at the time. 

Fluoroscopy is of no value at all in most cases of young children 
who cannot be managed in a totally dark room, asked to breathe 
deeply, cough, ete. The best is a roentgenographic plate, taken 
instantaneously, and studied after it has been developed. But even 
here we must be careful before concluding that because there is a 
shadow at the hilus, there is active tuberculosis of the intrathoracic 
glands. In nearly all infectious diseases of childhood, especially in 
scarlet fever, measles and whooping-cough, these glands are enlarged, 
but the swelling slowly retrogresses during convalescence. In fact, 
de Mussy attributed the paroxysms of cough in pertussis to enlarged 
glands. It is therefore hazardous to diagnose tuberculous adenitis in 
a child with whooping-cough, or scarlet fever, as I have seen done. 

Sluka! insists that several plates taken at long intervals are neces- 
sary, so that evanescent enlargements of the glands may be excluded. 
In fact, he found that the shadows shown on the plate of the same 
child at irregular intervals have been larger at one time and smaller at 
another; at times involving almost a complete lobe, or even a whole 
lung, at other times only a small circumscribed shadow was found; at 
one time in the right side, at other times in the left, etc. A consider- 
able part of these changes is due to changes in the collateral inflam- 
mation in active cases, but it seems to me that differences in the 
technic of taking the picture, the distance of the tube from the patient’s 
chest, the sharpness of the focus, the condition of the tube, ete., are 
responsible in many cases. 

On the whole there is no doubt that shadows in the region of the hilus 
are indicative of enlargement or engorgement of the glands in that 
region. This mottling and stippling of the hilus is, however, no 
criterionasto the activity of thedisease. Eventhe triangular or wedge- 
shaped shadow, with the base to the hilus, which has been described 
by Stoll and Heublein, Sluka, and others, is no proof of active disease, 
as the writer has repeatedly convinced himself. It appears also that 
in young infants these hilus shadows are only rarely seen even when 
adenopathy exists. Sluka says that in children under two years of 
age he never obtained a shadow on a chest plate which would even 
remotely suggest hilus tuberculosis, though he has taken numerous 
plates of sick children. He says that only during the third and fourth 
year do the glands begin to reveal themselves roentgenologically; they 
are mostly seen during the sixth and seventh years, and then begin to 
decrease in frequency. 

Of late the confidence formerly placed in x-ray findings in intra- 


1 Wien. klin. Wehnschr., 1913, 26, 254. 


470 PULMONARY TUBERCULOSIS IN CHILDREN 


thoracic conditions has been waning. At the 1915 meeting of the 
American Pediatric Society,! Koplik said that ‘one should be very 
cautious in permitting an a-ray to make a diagnosis for him.” Holt 
stated that he had “ sent the same case to a roentgenologist on successive— 
days and each day a different diagnosis was made. ‘The a-ray is very 
misleading and a dubious procedure upon which to base a diagnosis.” 

In doubtful cases the roentgenographic plate may give some indefinite 
information about the presence of enlarged thoracic glands. But when 
found in a child showing no clinical symptoms of the disease, we must not 
conclude that the child rs actively tuberculous. We do not as yet have 
enough experience with roentgenography in healthy children, nor have 
enough autopsies been made to verify roentgenographic findings, to 
warrant unequivocal conclusions. 

Tuberculin Diagnosis.— Basing their opinion on the fact that tuber- 
culosis in infants is almost invariably fatal, it has been concluded that 
when in a young child any of the tuberculin tests is positive, and there 
are some symptoms, such as cough, etc., the child should be pronounced 
tuberculous to the great dismay of the parents. I have seen children 
kept from school and thus deprived of an education, and perhaps 
hampered for the rest of their lives, solely because the von Pirquet 
reaction was found positive. 

We have already shown that the tuberculin reaction indicates but 
one thing—whether the person—child or adult immaterial—has ever 
been infected with tubercle bacilli. But it does not show conclusively 
whether the infection was followed by disease. Inactive infection 1s 
more likely to give a strong reaction than active tuberculous disease. 
In fact, in fatal tuberculous bronchopneumonia, meningitis, influenza, 
etc., the reaction is negative; in others it is but faintly positive. In 
other words, the stronger the reaction, the less likelihood of active or 
dangerous disease in the child, and a negative reaction is no positive 
proof of the absence of dangerous tuberculous disease. 

In infants under two years of age a positive reaction is to be taken 
as an indication of active disease because at that age infection is very 
likely to be followed by disease; during the first six months of life, 
almost invariably. But after two years of age harmless infections 
are the rule, so that the value of the tuberculin reaction acquires an 
academic importance, as was already shown, but it loses its clinical 
value. This is a point which pediatrists should bear in mind. It 
should never be lost sight of that after the third year latent tuberculosis 
is very common and this gives the same reaction as active disease. 

Diagnosis.—The diagnosis of tuberculous tracheobronchial aden- 
opathy depends on the presence or absence of clinical symptoms of 
disease. A child over two years of age showing a three-plus tuberculin 
reaction, and a shadow in the region of the hilus on the roentgenographic 
plate is to be considered well and healthy so long as it presents no 





1 Medical Record, 1915, 88, 502. 


TUBERCULOSIS DURING EARLY CHILDHOOD 471 


symptoms of disease; so long as there is no fever, no cough, no emacia- 
tion, etc. It is different with those who have clinical symptoms. 
In these it is always important to remember that when a child does 
not thrive, fails to gain in weight, the cause must be found. _ If it is not 
found, and there is cough, especially the dry, brassy cough, the tem- 
perature is to be taken three or four times a day. If an irregular fever, 
of the type described above is discovered, there is presumption of 
tuberculosis. However, children with enlarged tonsils and adenoids 
may cough and have subfebrile temperature for weeks. But it must 
never be lost sight of the fact that these children only rarely develop 
active tuberculosis, as is shown when discussing the lymphatic diathesis 
in relation to tuberculosis (see p. 588). If on examining the chest 
we find some dulness in one of the interscapular spaces, or anteriorly 
in the upper two interspaces near the sternum; and the whispered 
voice and the tracheal tone along the spine and in one or both inter- 
scapular spaces are audible in the peculiar characteristic fashion de- 
scribed when speaking of d’Espine’s sign, the diagnosis of tracheobron- 
chial adenopathy is clinched. 

It is different when these signs are found, even in conjunction with 
roentgenographic findings and a positive tuberculin reaction, in a child 
that shows no clinical symptoms of disease. There is no doubt that 
this child may have, and probably does have, enlarged bronchial 
glands. But these glands are not actively diseased, and so long as the 
little patient thrives, there is no cause for alarm. The glands are of no 
more clinical value than the scars found in the apices of 90 per cent 
of adults who die from causes other than tuberculosis; they are of no 
more serious import than the enlarged glands found on the necks of 
over 50 per cent of evidently healthy children in the slums of large 
cities. 

Prognosis.—The prognosis of tuberculosis in children under ten 
years of age embraces two problems: (1) The immediate outlook; 
and (2) the ultimate outlook. In other words, what are the chances 
of survival, or of retaining good health, immediately after infection 
has taken place, and is the child destined to develop phthisis after 
reaching the age of adolescence? 

The immediate outlook appears to be good, provided the lesions 
remain localized in the glands, or even in the bones and joints. This 
is clearly seen in cases of superficial glandular tuberculosis: Most 
children with tuberculous cervical adenitis, especially those requiring 
no operative interference, recover after a protracted illness. The 
same is true of osseous and articular tuberculosis. From 900 cases of 
tuberculous disease of the hip treated by A. Bowlby! at the Alexandra 
Hospital in London during twenty-one years, 33 died—a mortality of 
4 percent. He found that of the 33 who died, 24 were attacked by the 
disease before the age of six. The mortality from tuberculous tracheo- 


1 British Med. Jour., 1908, 1, 1465. 


472 PULMONARY TUBERCULOSIS IN CHILDREN 


bronchial adenitis is undoubtedly even lower. The greatest danger is 
metastasis in the meninges, but even this is comparatively infrequent 
after the fifth year. 

For this reason all methods of treatment of tuberculosis in children 
produce most excellent results. This is also the reason why orphan 
asylums—which harbor children between four and fourteen years of 
age—report that, despite the fact that most of their inmates are 
derived from the poorest strata of population, and an enormous pro- 
portion are of tuberculous stock, they have no morbidity nor mor- 
tality from tuberculosis. It is simply because death from tuberculous 
tracheobronchial adenopathy is extremely rare. The success of the 
open-air schools, the preventoriums, etc., should also be attributed 
in a great measure to this cause. 

Barring meningeal complications, or intercurrent acute infectious 
diseases, the prognosis in tracheobronchial adenopathy is excellent. 

In older children, seven years of age or more, the prognosis of 
apical pulmonary tuberculosis of the same type as seen in adults is 
more serious, though not so serious as in adults. It appears that 
pulmonary lesions in children heal with greater ease than in adults, 
though now and then we meet with a case in which the process in the 
lung proceeds to cavitation and the child succumbs to the usual clinical 
manifestation of phthisis. After the twelfth year there is hardly any 
difference in the clinical picture and prognosis of phthisis in children 
and in adults. 

Says Franz Hamburger,' one of the most experienced men in this 
field: ‘In general we can lay down the fundamental principle that the 
prognosis of tuberculous manifestations in children is not at all bad. 
It is, in fact, one of the most important achievements of recent years 
that we know: ‘Tuberculosis in children is a relatively harmless 
disease.’ It will naturally take decades till the lay public will learn 
this important fact.” And I may add till physicians in general will 
learn it. 

The prognosis depends on several other factors: The younger 
the child showing active tuberculous manifestations, the worse the 
outlook, the more liable it is to suffer from, or to suecumb to metas- 
tatic tuberculous manifestations, such as meningitis, rupture of a 
gland into a bronchus, the trachea, or esophagus. ‘These complications 
in fact become less frequent after the third year of life, and after the 
sixth year they are comparatively rare. The prognosis also depends 
on various accidental complications. ‘Thus, a child that escapes the 
endemic diseases, such as measles, whooping-cough, scarlet fever, 
diphtheria, etc., may grow up into healthy manhood, in spite of the 
enlarged g glands in the chest which disappear leaving harmless calcified 
foci in nenndy all cases after the tenth year; at any rate they give no 
more trouble. It is clear that the prognosis also depends on the 


1 In Brauer, Schréder and Blumenfeld, Handbuch der Tuberkulose, 1915, 5, 31, 


TUBERCULOSIS DURING EARLY CHILDHOOD 473 


social and economic conditions under which the child is raised. ‘Those 
who are well off in this regard have better chances to survive unscathed, 
because they have good nourishment, healthy dwellings, frequent 
vacations, and are less likely to contract other diseases, etc. 

The second element in the prognosis of tuberculosis during child- 
hood is the problem whether every child infected at an early age is 
destined to become phthisical after the fifteenth year of life. The 
facts observed in daily practice seem to be against such a view. If 
this were the case tuberculosis among adults would kill not only one 
out of seven to ten individuals, as is now found wherever there are 
available vital statistics, but over 90 per cent of humanity would 
succumb to phthisis. That an active tuberculous lesion during child- 
hood is not necessarily followed by phthisis in later life is evident from 
the following facts: 

We meet with many persons showing unmistakable signs of having 
had some form of tuberculosis during childhood, but pass through 
life as healthy and even vigorous individuals. This is the case with 
those showing scars on the neck which are undoubtedly remnants of 
tuberculous adenitis which had suppurated or was operated upon. 
We meet with many showing remnants of articular and osseous tuber- 
culous disease, yet they pass through life without developing phthisis. 
In fact, the contrary seems to be true. Those who see large numbers of 
phthisical patients are struck by the fact that consumptives with 
scars on the neck, or with ankylosis of joints following earlier tuber- 
culosis, ete., are extremely rare. This has been observed to be a fact 
by many clinicians, as is discussed elsewhere (see p. 584), and seems to 
indicate that an early tuberculous lesion may have some immunizing 
effect on the organism and prevent the development of phthisis in 
later life. 

We are, at the present state of our knowledge, not warranted in 
asserting that this protection against phthisis conferred by early 
tuberculous disease depends on infection with bovine tubercle bacilli, 
as some have been inclined to assume. But we may safely draw a 
conclusion that early tuberculous disease of the tracheobronchial glands 
is not necessarily followed by phthisis in later life, and there seems to be 
evidence that it may act in the same manner as articular, osseous, and 
glandular tuberculosis. 


CHAPTER XXV. 
PHTHISIS IN THE AGED. 


Frequency.— While discussing the frequency of tuberculosis during 
the various age periods we have shown that no age is exempt; in fact, 
it appears from available mortality statistics that after the age of 
twenty the death-rates from phthisis are about the same till very 
advanced life. While making autopsies pathologists are often struck 
with the frequency with which active tuberculous lesions are found in 
the lungs of aged persons, and investigations in homes for the aged show 
clearly that a large proportion suffer from phthisis. Thus, E. Braun! 
while making autopsies noted that in all bodies of persons over sixty 
years of age miliary tuberculosis was detected. The lungs were nearly 
always affected. In many the spleen, kidneys, and liver were involved; 
the meninges in only 10 per cent of cases. 

The reason why popular opinion has ascribed immunity of old 
subjects to phthisis appears to lie in the fact that, when occurring, 
this disease runs a mild, benign course and may pass off as bronchitis, 
asthma, ete. But when the sputum expectorated by senile persons is 
examined, it is very frequently found to contain large numbers of 
tubercle bacilli. In fact, these aged consumptives may be considered 
actual bacillus “carriers” who, without themselves suffering very 
much from the bacilli, disseminate the disease much more widely 
than younger patients who know of their condition and the danger 
of indiscriminate expectoration. 

Etiology.— Most phthisis in the aged has been acquired during 
childhood, but has been held in abeyance throughout life, to break out 
again at the period of life when the organs of the body begin to suffer 
as a result of wear and tear. Others have suffered from some form of 
phthisis before, but the disease was “cured,” to reawaken during old 
age. Many have been afflicted for years with some form of fibroid 
phthisis, but when senile degeneration began to manifest itself the 
tuberculo-fibroid lesions in the lungs began to activate with more vigor. 

From our present knowledge of phthisiogenesis we must exclude 
new infections of aged persons, because they have been infected during 
the earlier years of life, as was already discussed elsewhere. A new, 
or primary, infection in an adult would surely not pursue such a slow, 
sluggish course as is seen in the aged. The active disease in senile 
individuals should be considered either metastatic, or else old, perhaps 
dormant, processes flaring up and causing disease. 


1 Corr. Bl. f. Schweiz. Aerzte, 1917, 47, 1121. 


SYMPTOMS 475 


Pathologically, there are no differences in the lesions between the 
aged and those in adults in general, with but few exceptions. In the 
aged the fibroid processes predominate because the tendency to fibrosis 
of tissues is characteristic of advancing age. These fibroid formations 
tend to limit the lesion, prevent its spread and to surround the cavities, 
which show no tendency to enlarge by contiguity of the process. On 
the other hand, bronchiectatic cavities are more frequently found in 
older than in younger consumptives. 

Symptoms.—‘‘The conditions with which it may be associated 
modify the course of the tuberculous process,” says J. Edward Squires,! 
“so that the symptoms are obscured and the signs of its presence in 
the lung are somewhat indistinct. Tuberculosis, when it attacks lungs 
already damaged by the degeneration of age, may add but little to 
the discomforts of the individual who is already short of breath and 
‘wheezy.’ The increasing infirmity of the patient is accepted as a 
sign that he is ageing more rapidly, and no suspicion of any added mis- 
chief is aroused or entertained.” Generally speaking, the symptoms of 
phthisis in the aged are often those of fibroid phthisis, which have 
already been described. From most patients who consult us for hemop- 
tysis, cough, expectoration, and a lesion is discovered on physical 
examination, we elicit a history that they have been troubled with 
some of these symptoms for years, perhaps since childhood, but that 
they have been considered as suffering from chronic bronchitis or 
pulmonary emphysema. 

The patients cough, but the cough is mild. In aged persons the 
stimulus for cough is not so intense as in the young because the sensi- 
bility of the bronchial mucous membrane is greatly diminished. ‘The 
quantity of sputum they expectorate is, as a rule, not very consider- 
able because they have a tendency to swallow it. When told that 
they are tuberculous they are apt to resent the imputation, claiming 
that they have coughed for years, perhaps since they can recall, and 
if it had been “consumption” they would have succumbed long ago. 

Most senile patients are of slim build, but occasionally we meet with 
a tuberculous patient over sixty who is above the average weight. 
But with the onset of active symptoms they begin to lose in weight, 
and within a few months they may be reduced to mere skeletons. 

A large proportion of patients have no fever, though the methodical 
use of the thermometer per rectum may reveal a typical tuberculous 
temperature with slight rises, to 101° F. in the afternoon. In this 
respect phthisis does not differ from other diseases in the aged. We 
know that pneumonia may pass an afebrile course in the senile. The 
organism of the aged does not react with fever as does the body of 
the young. 

The pulse is more rapid than normal for the age of the patient. In 
rare cases tachycardia is seen, especially when there is cardiac dis- 


1 International Clinics, Sixteenth Series, 1906, 4, 90. 


476 PHTHISIS IN THE AGED 


placement. Dyspnea is a frequent symptom, especially after exertion. 
Because of the concomitant arteriosclerosis and myocarditis, cyanosis 
is not uncommon. In the later stages, when heart failure is apt to 
occur, edema of the extremities Is frequently seen. The blood-pressure 
is low considering the age and the condition of the arteries of the 
patient. Hemoptysis occurs quite frequently. In most cases it is 
merely streaky sputum, but it may be profuse and I have seen a fatal 
hemorrhage in a woman, aged seventy-eight years. Nightsweats are 
rare because, with advancing age, the sweat glands undergo atrophy, 
and also because the great oscillations of temperature characteristic 
of phthisis in the young are absent in the senile. 

A large proportion of aged tuberculous persons suffer from persistent 
diarrhea. In some it is very difficult to control by dietetic or medicinal 
treatment. Moreover, when the diarrhea is the dominant symptom, 
the symptoms and signs in the chest are overlooked, and a diagnosis 
of a gastro-intestinal disturbance is made. It is advisable that in all 
cases of persistent diarrhea in senile patients the chest should be care- 
fully examined, and inquiry made about the constitutional symptoms 
of phthisis. 

Physical Signs.—The appearance of the senile phthisical chest 
depends on the character of the lesions in the lungs. In those in whom 
there is pulmonary emphysema in addition to the tuberculous process 
there is the characteristic barrel-shaped chest, rigid, hardly expanding; 
in fact, always in the position of maximum inspiration. All that is 
seen is that the entire chest is lifted up with each inspiration, but there 
is no antero-posterior or lateral expansion. The intercostal spaces are 
wide and the direction of the ribs is more horizontal than normal. 
But many have no old emphysema and in them the thorax is rigid 
owing to the ossification of the costal cartilages; the ribs run at a 
more acute angle to the spine than normal and the intercostal spaces 
are wider; the supraclavicular and infraclavicular spaces are deeply 
excavated, more so on one side. During fits of coughing either apex, 
or both, may be seen blowing up in the supraclavicular space. Dilata- 
tion of the veins of the neck is a frequent symptom, and when there is 
relative tricuspid insufficiency, owing to dilatation of the right heart, 
there may be a venous pulse. I[yphosis and kyphoscoliosis are never 
absent. 

Auscultation is also not so satisfactory as in young subjects. The 
breathing 1 is superficial and, combined with pulmonary emphysema, 
which is only rarely absent, we may hardly hear any breath sounds! 
or only a feeble murmur is ‘audible. These are also the reasons why 
bronchial or cavernous breathing is so rarely heard over the sites 
of cavities. Bronchovesicular breathing of low pitch, with prolonged 
expiration may, however, be made out over one apex, at times, while 
carefully auscultating the chest. ales are not audible in many cases 
because of the superficial breathing; but over the sites of excavations 
large consonating rales may be heard, even when no breath sounds 


DIAGNOSIS 477 


are made out. At the base, these rales are usually due to bronchitis 
or bronchiectasis which are very frequent in old age. 

Course.—In many cases the cough, expectoration, emaciation, 
etc., continue for years and, inasmuch as these old persons do not 
follow occupations necessitating physical exertion, the true nature 
of the disease is not even suspected. They are considered patients 
suffering from chronic bronchitis or emphysema. I know old con- 
sumptives who have survived children and grandchildren whom they 
infected with tuberculosis. In fact, whenever I discover children with 
signs of tuberculous infection, though a history of exposure cannot 
be made out, I inquire for the grandparents, and have, in many 
instances, found that one of them was the source of infection, though 
he did not know the true nature of his illness. 

In the vast majority of cases the tendency of the disease is to pro- 
gress, though slowly, and never to a cure. Occasionally we find that 
it advances rapidly, assuming an acute or subacute course, with hectic 
fever, rapid emaciation, ete. Owing to the weakness and the general 
debility the cough is usually not at all severe, and when there is no 
fever, a diagnosis of carcinomatosis is made. Others cough and expec- 
torate for years, when suddenly fever develops and the patient is 
carried off within a few days. Bronchopneumonia may have been 
erroneously considered the cause of death, unless the sputum was 
examined and tubercle bacilli were found; a diagnosis of acute pri- 
mary tuberculosis may then be erroneously made. Daremberg speaks 
of acute phthisis in the aged, and Hoppe-Seyler speaks of acute miliary 
tuberculosis on rare occasions. But these cases are evidently acute 
exacerbations of chronic phthisis which had been kept in abeyance for 
years. The large proportion of cases of acute miliary tuberculosis 
found by Braun while making autopsies on aged persons show that it 
is frequently overlooked by clinicians. He points out that paradoxical 
bronchitis and bronchopneumonia, with signs of heart failure, doubt- 
less usually conceal the presence of acute miliary tuberculosis in the 
aged. 

Diagnosis.—The diagnosis is not difficult when the possibility of 
phthisis is kept in mind in all cases of cough, expectoration, emacia- 
tion, etc., met with in senile patients. Most of the mistakes made in 
these cases are due to failure to examine the sputum for tubercle 
bacilli. When the physical signs in the chest are indefinite, which is 
often the case, the bacteriological findings decide. When looking for 
fever in these cases we should never rely on the axillary temperature; 
only the rectal is to be taken. 

We must guard against mistaking signs of old, healed lesions for 
active disease. This can be avoided by a careful study of the symp- 
tomatology and bacteriology of the affection. 


LO) 5 By. od DU tad he, G9, tA As be 


TUBERCULOSIS OF THE PLEURA. 


THE serous membranes of the body, the meninges, the peritoneum, 
the pericardium, and the serous linings of the joints, are very much 
predisposed to tuberculous disease. As a serous membrane, the pleura 
is no exception in this respect. Indeed, it may be stated that tuber- 
culosis of the pleura is at least as common as tuberculosis of the lungs. 
In all forms of phthisis the morbid process extends from the pulmonary 
parenchyma to the visceral pleura. Its anatomical relations, blood 
supply, and lymphatics, render the pleura peculiarly liable to infection 
with tubercle bacilli which, as we have already shown, spread within 
the body either hematogenously or lymphogenously. Of the two 
sheets, the visceral, especially the part covering the pericardium and 
diaphragm, is very thin and firmly adherent, while the parts covering 
the surface of the lungs are thinnest and detached only with difficulty. 
The costal pleura is thicker and covered with flattened epithelial cells, 
while the cells covering the visceral pleura are less distinctly flattened, 
more granular and polyhedral. The pleura rests on a thin layer of 
subserous areolar tissue containing numerous elastic fibers. These 
areolar and elastic fibers are continuous with the elastic fibers and 
connective tissue within the lungs. 

The blood supply of the pleura is not an independent system, but is 
derived from two sources: The visceral pleura is, through its circula- 
tion, intimately connected with the lung, being supplied with branches 
of the pulmonary and bronchial arteries, but the capillaries beneath 
the visceral pleura form a coarser network than those of the pulmonary 
alveoli. On the other hand, the parietal pleura is supplied from the 
intercostal, phrenic, internal mammary, mediastinal and bronchial 
arteries. It is thus clear that disturbances in the bronchial and alveolar 
circulation may affect the pleura, especially the visceral sheet. More- 
over, inflammatory conditions of the lungs, when extending to the sur- 
face, will almost invariably implicate the visceral pleura, while the 
parietal sheet will only be affected through contact. 

The visceral pleura is very rich in lymphatic vessels and glands which 
are often visible to the naked eye. They are scattered all over the 
surface of the pleura, but are most numerous on the membrane cover- 
ing the interlobar fissures. Their connection with the bronchial glands 
is evidenced by the fact that they too became darker in older indi- 
viduals owing to the deposition of carbon particles brought into the 
lungs with the inhaled air. The lymphatics of the parietal pleura pass 
to small intercostal glands situated near the heads of the ribs, and 


PATHOLOGY 479 


indirectly, through their connection with the lymphatics of the fourth 
and fifth intercostal spaces, with the axillary glands. There are also 
communications between the lymphatic systems of the chest and the 
abdomen through anastomosis between the lymph vessels of the pleura 
and those of the peritoneum, particularly that covering the lower sur- 
face of the diaphragm. At first sight a closed cavity, the pleura is thus 
seen to communicate through its bloodvessels and lymphatics, in 
the latter by means of stomata, with the air inhaled into the lungs 
as well as with the abdomen. Infection of any part of the lungs or its 
glands, or of the peritoneum, is likely to spread hematogenously or 
lymphogenously to the pleura. In fact, experimental investigations 
of Grawitz, Grober, Fleiner, and others, have shown conclusively that 
coloring matter insufflated into the lungs of animals was subsequently 
found in the pleura. Tubercle bacilli carried by the blood, or especially 
the lymph stream, may thus produce pleurisy even if the lungs remain 
unaffected. Primary tuberculous pleurisy is thus explained. 

The lymphatic connections of the pleura have recently been studied 
in this country by William Snow Miller... He found that the 
lymphatics of the pulmonary parenchyma drain directly into the 
bronchial lymph glands. But the pleura has a set of lymphatics 
entirely distinct from those of the lung substance proper. In the 
injected specimen they appear as a network of rather large lymphatic 
vessels, in the meshes of which are numerous smaller vessels. This 
pleural lymphatic system has an independent drainage of its own 
directly into glands at the hilus, except for the diaphragmatic pleura 
of the lower lobes which drains into the preaortic nodes wa lymph 
vessels in the ligamentum pulmonale. The valves of the lymphatics 
leading from the pleura point toward the hilus and prevent the flow 
of lymph in the reverse direction. It is important to note that there 
is a connection between the lymphatic systems of the pulmonary 
parenchyma and the pleura by means of short lymphatic trunks which 
follow the branches of the pulmonary veins that take their origin from 
the pleura. The valves in these communicating lymphatics all point 
toward the pleura, so that the lymph in these vessels must always flow 
from the lung tissue toward the pleura, and not vice versa. The bear- 
ings of facts with respect to the lymphogenous transmission of tubercle 
bacilli, or other organisms, or even cancer cells, are obvious. 

Pathology.— While making autopsies on tuberculous bodies we almost 
invariably find that the pleural sheets, in part, or even completely, are 
covered with fibrinous exudate, a false membrane; are adherent at 
some circumscribed area, or more extensively, and thickened. 

An exudate in which fibrin filaments are more or less abundant is 
frequently found within the pleural cavity. In nearly all cases of 
chronic phthisis the pleural sheets over the affected upper lobe are 
thick, and densely adherent, so that the lung cannot be removed 


1 Am. Rey, Tuberc., 1919, 3, 33. 


480 TUBERCULOSIS OF THE PLEURA 


without force; either the parenchyma, or the tissues on the inner side 
of the chest wall, must be forcibly torn or cut for the purpose. Next in 
frequency, thickening and adhesions of the interlobar and diaphrag- 





Fig. 100.—Tuberculous pleural adhesions. At the lower part of the drawing is to be 
noted that the subcostal cellular tissue is very much reduced in quantity. Above it 
the new membrane is developed at the expense of the visceral pleura and shows a layer 
of tuberculous follicles. The fibrous tissue gradually extending upward and coming in 
contact with the lung without any sharp line of demarcation between them, is already 
old, well organized in parallel bundles and passed by numerous bloodvessels. (Chante- 
messe and Courcoux.) 


matic pleure are found. The interlobar fissure near the affected part 
is thus often obliterated. In acute cases miliary tubercles may be 
found scattered all over the surface of the pleura; in others tuberculous 
neoformations occur; they may form large villous tumors which, in 


PRIMARY TUBERCULOSIS OF THE PLEURA 481 


rare instances, are found pedunculated as in bovine tuberculosis of 
the pleura. Very often calcified areas are made out in the affected 
part of the pleura which, at times, may be over one centimeter in thick- 
ness, and converted into a fibrous or even calcified mass which sur- 
rounds the diseased and excavated part of the lung like a solid shell. 

Microscopically the false membrane in mild cases is made up of fibrin 
enmeshing red blood corpuscles and round cells. The pleura proper is 
invaded by young connective-tissue cells, tuberculous granulations, 
epithelioid and giant cells, and areas of caseation. The adjacent paren- 
chyma of the lung usually shows atelectasis of the alveoli, vascular 
dilatation and proliferation of the epithelial cells. 

In a certain sense, the implication of the pleura in pulmonary tuber- 
culosis may be regarded as a protective process. The acute symptoms 
of pleurisy, especially the pain in the chest, impede the motion of the 
affected part of the thorax and thus afford rest to the diseased lung, 
favoring cicatrization of thelesion. But this is of less significance when 
compared with the protection pleural adhesions afford the patient 
against loss of continuity of the visceral pleura resulting in pneumo- 
thorax. When the tuberculous process reaches the cortical surface of 
the lungs, which it does in nearly all active and progressive cases, a 
minute caseated area will permit the entry of air into the pleura and 
cause collapse of the lung. The pleural adhesions over the site of the 
lung lesion prevent this accident in over 95 per cent of cases of phthisis. 

Varieties of Tuberculous Pleurisy.—The following forms of tuber- 
culous pleurisy may be differentiated clinically and pathologically: 

1. Primary tuberculosis of the pleura, which is rare. 

2. Pleurisy during the course of acute pulmonary tuberculosis. Met 
with in nearly all cases. 

3. Pleurisy during the course of chronic pulmonary tuberculosis, 
encountered in various degrees of intensity and extent in nearly all 
cases of chronic phthisis. 

Each of these forms of pleurisy may be dry or moist. The latter 
class may have serous, serofibrinous, sanguineous, or purulent effu- 
sions. It may be unilateral or bilateral; may involve the entire 
surface of the affected pleura, or only a limited area. 


PRIMARY TUBERCULOSIS OF THE PLEURA. 


Primary tuberculosis of the pleura is rare, if it occurs at all. It is 
clear that in such cases the virus must be brought to the pleura through 
the blood or lymph stream. Experimental investigation has shown 
that even when the pleura is directly inoculated in a healthy animal 
no local tuberculous lesion is produced. Cleveland Floyd! found that 
only when the pleura is sensitized by a previous infection for some days 
the response to infection with pyogenic microdrganisms was in the 


1 Tr. Am. Climatol. Assn., 1914, 30, 205. 
31 


482 TUBERCULOSIS OF THE PLEURA 


nature of purulent effusion. Similarly, Robert C. Paterson! found that 
fluid is never produced by a primary inoculation of the pleura with 
tubercle bacilli. But in tuberculous animals inoculation of tubercle 
bacilli produces an exudate of serum, leukocytes, red blood corpuscles, 
and fibrin. He therefore arrives at the conclusion that clinical pleural 
effusions are caused by infection of an “allergic” pleura; in other words, 
that they are due to reinfections from within, or from without the body. 
This is confirmed by the clinical observation that pleural effusions are 
almost invariably preceded by many months, or years, by tuberculosis 
of some other organ in the body, notably the lung, the lesion remaining 
dormant. Pathologically also there are confirmations—in nearly all 
cases of tuberculous pleurisy that come to autopsy older lesions are 
found in the lungs, or the intrathoracic glands. 

Tuberculous pleurisy is found more frequently in men than in 
women. While no age is exempt, it is mostly found in adults. Pleurisy 
in children, with or without effusion, is, as a rule, non-tuberculous. 
Many patients give a history of exposure to cold as the immediate 
exciting cause. Whenwe bear in mind thatit isan endogenous reinfec- 
tion with tubercle bacilli, we can readily conceive that exposure to 
cold may prepare a suitable soil for the tubercle bacilli brought there 
by the blood, or by contiguity to adjacent diseased organs. The 
blood and lymph supply of the parietal pleura, being derived from 
that of the chest wall (see p. 478) will predispose it to inflammation 
after chilling of the chest wall. It may be stated, however, that 
the vast majority of these cases of “idiopathic” pleurisy are tubercu- 
lous. Autopsies made on persons with dry pleurisy, apparently 
due to “colds,” have shown distinct tuberculous lesions of the lung and 
pleura. At times an injury is responsible for the onset of pleurisy. 
But it appears that individuals who do not harbor tubercle bacilli, or 
are otherwise not predisposed to tuberculosis, do not develop tuber- 
culosis of the pleura after an injury to the chest. During the 
World War tuberculosis of the pleura was noted to follow injuries 
and wounds of the pleura only in exceedingly rare instances. 

Symptoms of Dry Pleurisy.—In general practice dry pleurisy is 
very frequently observed. After exposure, or without any known 
provocative cause, the patient is seized with some chilly sensations, 
though the acute chill characteristic of pneumonia is very rare, becomes 
feverish, has pain in the side of the chest, and more or less dyspnea. 
Unproductive cough is almost invariably present, and it aggravates 
the dyspnea and the pain. In some instances paroxysmal attacks of 
cough occur which are very painful. Physical examination of the chest 
shows diminution of mobility, at times almost complete immobility, 
of the affected side of the chest. Percussion yields negative results, 
but auscultation reveals a dry friction sound, most commonly in the 
region where the pain is acutely felt—the lower part of the chest in the 


1 Am, Rev. Tuberc., 1917, 1, 353, 


PRIMARY TUBERCULOSIS OF THE PLEURA 483 


anterior axillary line, or the mammary region, or behind, in the region 
of the angle of the scapula. In some cases the pain is mild, but in others 
it is severe, lancinating. It may be relieved, more or less, by anything 
which tends to immobilize the affected side of the chest, and is aggra- 
vated by deep breathing, or coughing. 

As has been pointed out by Capps, the pain in pleurisy is only felt 
superficially; it is “referred,” and can be elicited only in the skin, sub- 
cutaneous tissue, and muscles. The sensitized area is hyperesthetic, 
hyperalgesic, and often characterized by painful tender points. The 
muscular cutaneous reflexes are exaggerated, and can best be elicited 
by striking or pinching the skin. In most cases it is felt in the region 
of the affected pleura, 2. e., where the friction sound is heard; tender- 
ness of the intercostal spaces may be elicited. 

In diaphragmatic pleurtsy no friction sounds are heard on auscultation 
and the diagnosis is made mainly by a consideration of the general and 
local symptoms. The fever is, in most cases, high and the dyspnea 
severe owing to the immobility of the affected half of the diaphragm, 
the result of the pain which may be agonizing. It is aggravated by 
cough, swallowing and abdominal breathing. For this reason the 
patient makes a strong effort to breathe mostly with the upper part 
of his chest, thus keeping his diaphragm at rest as far as possible. 
The diaphragm derives its sensory nerve supply from two sources— 
the phrenic, and the last six intercostal nerves. The central portion 
of the diaphragmatic pleura is innervated by the phrenic nerve. 
Hence, inflammation of the central portion sets up pain in the neck, 
at the crest of the shoulder, corresponding to the cutaneous distribution 
of the fourth cervical nerve, which has its center in the spinal cord at 
the same level as the phrenic. The periphery of the diaphragmatic 
pleura is innervated by the sensory fibers of the intercostal nerves and 
inflammation of that area gives rise to referred pain in the lower thorax, 
the lumbar region, or the abdomen. These points of tenderness in 
pleurisy were first studied by Gueneau de Mussy,! who described 
boutons diaphragmatiques, points of maximum tenderness at the inter- 
section of the parasternal line and a horizontal line continuous with 
the end of the tenth rib. More recently Sir James Mackenzie,? and 
especially Joseph A. Capps,’ have carefully studied the subject. 

In many cases of diaphragmatic pleurisy the referred pain over the 
abdomenand back (Figs. 101 and 102) is not unlike that due to appendi- 
citis, gastric ulcer, cholelithiasis, and other intra-abdominal diseases. 
Capps mentions cases in which such errors have been committed; Lewis 
Sayre Mace reports several in which gastric ulcer was diagnosticated, 
and I have seen many cases of this type, especially in tuberculous 
patients who have had recurrent attacks of diaphragmatic pleurisy and 
resulting adhesions. 


Arch. gén. de méd., 1853, 2, 271; 1879, 2, 141. 
Symptoms and Their Interpretation, London, 1910. 
Arch. Int. Med., 1911, 8, 717; Am. Jour. Med. Sci., 1916, 151, 333, 


o nm ie 


484 TUBERCULOSIS OF THE PLEURA 


T. H. Kelly and H. B. Weiss! report a series of cases of diaphragmatic 
pleurisy which simulated surgical conditions so closely that the ques- 


{| 


ii gl 





Fia. 101.—Points of maximum pain and tenderness in abdomen and back occurring in 
61 cases of diaphragmatic pleurisy. (Capps.) 





lia. 102.—Points of maximum pain and tenderness in the neck region occurring in 
61 cases of diaphragmatic pleurisy. (Capps.) 


1 Am, Jour, Med. Sci., 1918, 156, 808, 


PRIMARY TUBERCULOSIS OF THE PLEURA 485 


tion of operative intervention was seriously considered. Among the 
diseases which required differentiation were renal stone, acute chole- 
cystitis, generalized acute peritonitis from perforated typhoid ulcer, 
etc. Some had in fact been operated upon for appendicitis and gall- 
bladder disease previous to coming under Dr. Kelly’s observation. 
In none of those operated cases was stone or any other pathological 
condition of the intra-abdominal viscera found at the operation, and 
shortly afterward there was a recurrence of the symptoms that had 
existed before the operation. 

Several cases of diaphragmatic pleurisy have come under my obser- 
vation in which the diagnosis was made of chronic recurrent appendi- 
citis, and operated upon; others in which operation was performed for 
gastric ulcer because of hemorrhages which in reality were due to 
tuberculous lesions in the lung, or bronchiectasis which is not uncom- 
mon in chronic diaphragmatic pleurisy. One patient with a thick 
pleura over the right base was operated upon four times: For appendi- 
citis, for gall-stones, for gastric ulcer, and finally for “adhesions.” 
When he came under my observation he still had pain in the right side 
of the abdomen, and a surgeon urged another operation. We have 
already shown that hematemesis is at times difficult of differentiation 
from pulmonary hemorrhage (see p. 251). In tuberculous patients, 
symptoms of appendicitis, especially of the chronic and recurrent type, 
should be carefully analyzed before a final opinion is given. 

The differentiation may be attempted along the followi ing lines: In 
diaphragmatic pleurisy there are two areas of tenderness on pressure: 
One posteriorly along the twelfth rib of the affected side; the second 
at the ridge of the trapezius. Spontaneous pain at these points may 
occur, but pressure elicits it in nearly every case. In some instances 
there is observed pain and rigidity of the abdominal muscles of the 
affected side. When due to intra-abdominal disease deep pressure 
will produce severe and deep-seated pain. ‘The pain is greatly increased 
when the patient breathes deeply with the abdomen. When the pain 
over the abdomen is “referred,’’ due to diaphragmatic pleurisy, deep 
pressure with the flat surface of the fingers is well borne, only cutaneous 
hyperalgesia is present; and pinching the skin, or slightly stroking it, 
will elicit tenderness and pain. In chronic cases careful physical 
exploration of the chest will show, in most instances, signs of a thick 
pleura. In acute cases, the sudden onset, the severe pain in the 
chest and shoulder and other characteristic symptoms of pleurisy, when 
combined with absence of a friction sound, point to diaphragmatic 
localization of the lesion. 

Inrare cases of diaphragmatic pleurisy the diaphragm on the affected 
side is relaxed and strikingly elevated, and the most annoying symptom 
is uncontrollable hiccough. 

Interlobar dry pleurisy of a tuberculous nature also occurs at times 
No frictions are audible, as a rule, but feeble breath sounds are found 
while listening over the lung above the fourth or third rib, owing to 


486 TUBERCULOSIS OF THE PLEURA 


immobilization of the lung above the affected part of the pleura. This 
form of pleurisy is apt to recur, as has been shown by Piéry, and after 
several attacks the lung is implicated in the tuberculous process. 
These cases of recurring interlobar pleurisy, as well as apical pleurisy 
which will soon be described, are characterized by symptoms of 
incipient phthisis without the pathognomonic physical signs and with 
negative sputum. Even if after several attacks the parenchyma is not 
implicated, the after-effects may be disagreeable, particularly when 
the lesion is in the left side of the chest. The thick pleura and the 
adhesions remain permanently and the cicatrix may contract. By 
their attachment to the mediastinum they may pull the heart out of 
its normal location outward and upward and thus hamper its action 
I have seen cases of this type in which no signs of excavation, or even of 
infiltration, of the left lung could be discovered, yet the heart was 
displaced, and the dyspnea, tachycardia, acrocyanosis, and debility 
were so pronounced as to completely disable the patient, even though 
there was no active parenchymatous lesion to be discerned, and the tem- 
perature had been normal for along time. While most of these patients 
are below normal in weight, I have seen many who were quite corpulent, 
and the obesity contributed to their misery. The diagnosis is made 
from the history of repeated attacks of pleurisy, cardiac displacement 
and, very frequently, the absence of breath sounds over the upper 
third of the affected lung. Many of these cases are considered as non- 
tuberculous apical lesions. The thick interlobar pleura may at times 
be.seen as a sharp line in the roentgenogram, and considered as an 
indication of a cavity. In fact many of the “annular shadows” (see p. 
365) are produced by thickened interlobar plura. 

Apical pleurisy is another variety of tuberculous disease limited 
to a portion of the pleura which is not generally appreciated to the 
extent it deserves. Many cases of tuberculosis with negative sputum, 
as well as doubtful cases in general, are in fact apical pleurisy which 
is not properly diagnosticated. Emil Sergent! and M. T. German? 
have recently made a careful study of this condition and shown that 
it occurs more frequently than it is diagnosticated. 

It has already been shown that the pleura covering the apex of the 
lung is almost invariably implicated in cases of tuberculous lesions of 
the upper lobe of the lung. But at times the pleural lesion is, in the 
clinical sense, primary, and its symptoms precede those of the pul- 
monary lesion, or it is not at all followed by an apical process. The 
symptoms presented are suggestive of phthisis, but physical examina- 
tion and roentgenography fail to elicit conclusive signs of a localized 
lung lesion, and the patient is either pronounced non-tuberculous, 
treated as a case of incipient phthisis with negative sputum, considered 
as suffering from some non-tuberculous apical lesion, etc. Many 


1 Presse médicale, 1916, 24, 369. 
2 Btude sur le syndrome de la pleurite apicale dans le tuberculose pulmonaire, Thése 
de Paris, 1916-17, No. 30. 


PRIMARY TUBERCULOSIS OF ‘THE PLEURA 487 


cases of abortive tuberculosis (see p. 414) are in fact tuberculous apical 
pleurisy. 

The onset is insidious. The patient is troubled with mild fever, 
unproductive cough, pain in the chest or shoulder and, coupled with 
anorexia, there is observed a constant loss in weight, though rapidly 
progressing emaciation is uncommon. I have also noted that the 
tachycardia characteristic of phthisis is lacking in most cases. Physical 
examination of the chest shows either slight or no impairment of reso- 
nance over the affected area during the early period of the illness. On 
auscultation the breath sounds are diminished or abolished; in some 
cases cog-wheel breath sounds are heard. Auscultation yields one sign 
which is characteristic: A friction sound is heard in the supraspinous 
fossa of the affected side of the chest. Its location is usually the 
“alarm zone,’ which has already been described (see p. 379). This 
triction sound is heard as occurring very superficially, and it is diffi- 
cult to differentiate it from crepitation. It is heard only for a few days 
and disappears, to reappear during an exacerbation of the process. 
Its characteristics have been well described by Thomas Clifford 
Allbutt:! “Its significance cannot be overrated. It is far from an 
axiom to say that a streak of pleurisy, audible at the apex, means 
pulmonary tuberculosis.” It is recognized by an elusive apical rub, 
“as if it were rather a creaking of a stiff membrane than a translation 
of surfaces.’ A faint creak may be all that is heard; it is often simu- 
lated by some fortuitous little wheeze or chirp. 

The following guides may be of service in differentiating this rub 
from crepitation: With crepitation there is almost invariably some 
alteration in the breath sounds, which are either bronchovesicular or 
bronchial, while with a friction sound they are either feeble, or com- 
pletely abolished; exceptionally there are cog-wheel breath sounds. 
Cough will accentuate crepitation, rarely abolish it, while a friction rub 
is not influenced by it. In most cases frictions are audible during 
both the inspiratory and expiratory phases of respiration, while 
crepitation is only heard during inspiration. 

Sergent? has pointed out two other symptoms of apical pleurisy 
which are of great assistance in the diagnosis. They are: (1) In- 
equality of the pupils; (2) swelling of the glands in the supraclavicular 
fossa. ‘These two signs may be found singly or in combination. 

Inequality of the pupils is observed very early, and when found in a 
patient who coughs and shows a friction rub in the supraspinous fossa 
is to be taken seriously. The pupil on the side corresponding to the 
affected pleura is somewhat dilated. It is best observed when the 
patient is made to fix his gaze upon a distant dark object and it dis- 
appears when a strong light provokes a strong contraction of the iris. 
The extent of the pupillary dilatation varies from day to day, and in 
some cases it persists after the pleural lesion has healed. 


1 Lancet, 1912, 2, 1485. 
2 Fitudes cliniques sur la tuberculose, Paris, 1919, pp. 102, 581, 595. 


48S TUBERCULOSIS OF THE PLEURA 


The enlarged supraclavicular glands are mainly found in the angle 
formed by the inner extremity of the clavicle and the sternal tendon 
of the sternocleidomastoid muscle. If they are enlarged, light palpa- 
tion of that region will reveal these glands in most cases. In patients 
with large muscles of the neck palpation must be done delicately while 
the patient has his muscles relaxed by bending his head toward the 
affected side. The swelling of these glands occurs late, after the disease 
has lasted for some time. In fact, when it does occur there are, as a 
rule, already signs of a parenchymatous lesion in the apex, at times even 
positive sputum. Occasionally the swelling is quite marked, but in 
most cases it is insignificant and requires careful palpation of the 
region before it is appreciated. Moreover, we must be careful before 
pronouncing palpable structures as enlarged glands. ‘The tendon of 
the omohyoid, or the external jugular, may be mistaken for enlarged 
glands. 

In a large proportion of cases patients also complain of pain in the 
shoulder or the back beneath the scapula. This is usually a dull pain, 
uninfluenced by respiration, cough, or the position of the body. 

The course of apical pleurisy is mild in most cases. The patient 
coughs for some weeks or months and recovers. When the cough, 
fever, pain, etc., have disappeared the patient may feel well indefinitely, 
but on percussion we find that the resonance over the affected apex 
remains impaired and the supraclavicular fossa is more or less deeply 
excavated. ‘The breath sounds remain feeble, or some sibilation may be 
audible. It is clear that these signs are indications that the pleura in 
that region has remained thick and adherent. ‘Though no relapse has 
occurred, these patients are often erroneously diagnosed as tuberculous 
when they have common colds, or some other non-tuberculous respira- 
tory affections, and the physician carefully examines the chest. Roent- 
genography may confirm the diagnosis of phthisis by showing a distinct 
narrowing of the pulmonary field and some opacity of the apical paren- 
chyma; the so-called ground-glass appearance is very commonly seen, 
owing to thickening of the pleura and cicatricial contraction of the apex. 
But, as has repeatedly been stated, only constitutional symptoms 
should decide in these borderland cases whether the patient is sick 
with active phthisis requiring treatment. 

Apical pleurisy is likely to recur. In some patients under my care 
there have been several relapses at irregular intervals, until finally the 
symptoms of pleurisy merged into those of active pulmonary tuber- 
culosis—the process invaded the parenchyma and symptoms and 
signs of an apical lesion could be made out. It is among these cases 
that strictly localized lesions are encountered—the parenchyma may be 
completely destroyed in the upper lobe, leaving a dry cavity, and the 
patient recovers. The sharp line of demarcation between the diseased 
portion of the lung and that which has not been infected is clearly 
seen on the roentgenographic plate. The thickened interlobar pleura 
apparently limits the progress of the lesion. In others the lesion 


PRIMARY TUBERCULOSIS OF THE PLEURA 489 


extends, may invade the other lung, and chronic phthisis of the usual 
type pursues its course. 

In the majority of cases, however, tuberculous apical pleurisy pursues 
a very benign course. The patient has slight fever for a few weeks, 
coughs for a variable period without expectorating, has slightly en- 
larged glands above the clavicle, and inequality of the pupils, while aus- 
cultation shows a friction rub over the supraspinous fossa. Within a 
few weeks to three months recovery may be complete, though there is 
likelihood of a recurrence of the trouble. 

Primary Pleurisy with Effusion.—A pleural effusion is very com- 
monly the first indication of phthisis. Numerous patients give a 
history of fairly good health when, after exposure, they were laid up 
with cough, fever, pain in the chest, dvspnea, etc. Within a few days 
physical exploration of the chest shows the presence of fluid in the 
pleura which is confirmed by an aspirating needle. It is not rare to 
meet with patients who say that they have felt out of sorts for some 
weeks, perhaps they have coughed somewhat, or have been slightly 
short-winded and unable to pursue their usual vocations efficiently, 
but still they have thought little of it. An examination reveals an 
effusion in one side of the thorax, though at no time have they had pain 
in the chest. 

It is important in these cases to inquire carefully into the history of 
the patient. A large proportion of these ‘“primary”’ pleurisies are in 
fact secondary to long-standing, but unrecognized, phthisis. While the 
patient says that he had felt quite well, interrogation often elicits the 
information that he had coughed for many weeks or months before 
the onset of the symptoms of pleurisy; perhaps that he had hemop- 
tysis many months or years before, but had completely recovered. 
In fact, his physician had told him that the symptoms indicated 
merely a trifling derangement, a “cold,” gastritis, neurasthenia, etc. 
But with the arrival of the new symptoms—the painful cough, the 
fever, the pain in the chest, the dyspnea—things took a different 
aspect. It is thus clear that the patient has been tuberculous for a 
long time, and only with the arrival of the symptoms of pleurisy with 
effusion he decided that he must be carefully examined. Under the 
circumstances, a patient with pleurisy who has been ailing for some 
time before the arrival of the acute symptoms is to be considered 
tuberculous and treated as such. 

I have observed a certain number of cases of pleurisy with effusion 
which began with hemoptysis. In fact, in several cases the disease was 
ushered in with a profuse hemorrhage. All these turned out to be 
tuberculous. In one case the effusion was absorbed and the patient felt 
well for five years and then developed phthisis. It has been my 
practice to consider all pleurisies accompanied by hemoptysis as 
tuberculous. 

The temperature of the patient is in most cases high, 102° to 104° F. 
is not uncommon. It is usually slightly remittent in type; during the 


490 TUBERCULOSIS OF THE PLEURA 


morning hours it may be one or two degrees lower than during the after- 
noon or evening. It is not due altogether to the absorption of toxins 
from the effusion, but appears to be the reaction of the body, against 
the invading enemy. In fact, the young, the vigorous, have higher 
fever than the weak, the decrepit and the aged, and in many cases the 
fever abates long before the absorption of the fluid. The fever is 
accompanied by the usual symptoms of pyrexia, anorexia, backache, 
insomnia, ete. After remaining high for about one or two weeks there 
is shown a tendency to a decline in the temperature, and within three or 
four weeks the patient may be completely afebrile, irrespective of the 
presence or absence of fluid within the pleural cavity. 

The pulse is accelerated in nearly all cases, corresponding to the 
degree of the fever. In some cases tachycardia is severe, and a pulse- 
rate of 120, or more, is observed. The cyanosis, which is common to 
some degree in nearly all cases, may then be appalling. In rare 
instances in which failure of the circulation is accentuated there may 
be edema of the extremities; unilateral edema of the face, arm, chest, 
and leg, corresponding to the affected side of the pleura is occasionally 
observed. 

Dyspnea is another symptom which is not lacking in most cases. 
In some it is merely objective. Though the patient believes that he is 
not short winded, we clearly see that he is, and the respirations are 
found thirty or forty per minute. During the first few days the 
dyspnea is often due to the pain, while later the pleural effusion, 
cardiac displacement, and weakness are responsible. With the begin- 
ning of absorption of the pleural fluid the dyspnea lets up and finally 
disappears when complete absorption has taken place. 

Physical Signs.—A physical exploration of the chest shows that the 
affected hemothorax is larger than its mate, the intercostal spaces 
obliterated and, when the exudate is copious, they may even bulge out. 
This is in contrast with the average phthisical chest in which the inter- 
costal spaces are deeply indented and there are inspiratory retractions 
to be observed. Inspection may also show the sign of the spinal muscles 
which has been described by Felix Ramond.! On the affected side 
the erector spine is in a state of permanent reflex contraction. On 
inspection the muscular mass on the affected side appears to be more 
prominent and broader than on the sound side. On palpation the 
muscles give a sensation of hardness and resistance which may be com- 
pared to that of India-rubber slightly stretched, which differs markedly 
from the sensation elicited in the muscles on the sound side. _ If disease 
of the spine is excluded, this is a fairly reliable sign of an effusion into 
the pleura. Very small effusions, which escape physical diagnosis and 
even roentgenography, may thus be detected. 

Percussion elicits a flat note over the site of the effusion, while above 
the level of the fluid the note is tympanitic, owing to relaxation of the 


1 Bull. et mém. Soc. méd. d. hép. de Paris, 1910, 29, 747. 


PRIMARY TUBERCULOSIS OF THE PLEURA 491 


atelectatic lung tissue immediately above the upper level of the fluid. 
When the amount of fluid is small, under 500 ce, it cannot, as a rule, 
be detected by percussion, excepting in rare instances of very small 
and emaciated chests. But tidal percussion, showing immobility of 
one-half of the diaphragm, is suggestive when the symptoms point to 
pleurisy. ‘The various lines described by Garland, Ellis, and Demoi- 
seau may be made out by light percussion along the upper level of the 
fluid (Figs. 103-105). One important sign is flatness above the left hypo- 
chondrium, ‘Traube’s space, in effusion into the left pleura. In two 
out of three cases small effusions may be detected there early, but 
there are some important exceptions: It remains resonant, or tym- 
panitic, in one out of three cases of moderate effusion. In small 
women with narrow chests a small effusion of about 1500 cm. of fluid 
may efface that space, but in large men with capacious chests a large 
effusion may leave it with clear resonance, especially when the patient 
has been kept in bed for several days and the fluid sank to the posterior 
aspects of the pleural cavity. I have observed many cases in which 
the effusion was copious, but because of old adhesions and thickening 
of the anterior aspect of the pleura, there was no sinus into which the 
fluid could penetrate anteriorly and it only filled up the chest poste- 
riorly. On the other hand, in some cases of effusion into the right 
pleura, Traube’s space is dull or flat on percussion owing to displace- 
ment of the left lobe of an enlarged liver downward and to the left. 
The upper level of the effusion may be made out easily by light per- 
cussion. It will be found that no straight horizontal line can be drawn 
as in hydropneumothorax when the patient is in the upright position. 
As was shown by Calvin Ellis, of Boston, in 1873, “when a pleural 
effusion is small, it may occupy a conical section of the pleural cavity in 
the subaxillary region, where respiration and resonance may be wanting. 
But in a certain number of cases, when the effusion is quite large, if an 
accurate line be drawn, the flatness will be found to describe a curve 
gradually approaching the spine toward the base of the chest, leaving a 
space from one to three inches broad between the spine and the line of 
flatness. In this space resonance will still be detected and respiration 
heard.” George W. Garland, experimenting on animals, confirmed the 
tendency of fluids in the pleural cavity to form a curved outline, the 
highest point of which is in the midaxillary or scapular region, declining 
as it proceeds forward on the anterior wall of the chest, and to a lesser 
degree on the posterior aspect (Figs. 103, 104and 105). Of the various 
explanations which have been given for this curved line indicating the 
upper level of the effusion, the most plausible appears to be that while 
attempting to make room for itself, the fluid will compress the least 
resisting parts of the walls of the pleural cavity. The mediastinum, 
which is very mobile when not held by strong adhesions, is pushed to 
the opposite unaffected side. After this has reached its limits the lung 
will be compressed. At its roots the lung is held strongly, but at the 
sides the spongy tissue, when not held by adhesions, is easily com- 


492 TUBERCULOSIS OF THE PLEURA 


pressible and by retraction will recede, permitting the fluid to accumu- 
late more along the sides of the pleural cavity. Tor this reason Gar- 





I'ia. 103.—Ellis’s line in pleural effusions. Fie. 104.—Ellis’s line in pleural effusions. 





Fie. 105.—Ellis’s line in pleural effusions. 


land’s line is only found in large effusions; when there is but little fluid, 
the upper level is practically horizontal. Moreover, this curve can only 


PRIMARY TUBERCULOSIS OF THE PLEURA 493 


be mapped out when the patient is in the erect posture; lying down 
produces a change in the line indicating the upper level of the fluid. 
In patients who walk around the line described above may be lacking— 
the upper level of the fluid is almost horizontal. 

Many authors speak of shifting of the upper level of the fluid accord- 
ing to the position of the patient, and some say that it can be demon- 
strated in most cases. But experience has taught me that it does not 
occur in pleurisy, and when it is found we are dealing with hydropneu- 
mothorax. The outlook here is quite different from that in sero- 
fibrinous pleurisy. Recent investigations of this subject by H. Kk. 
Dunham! with the aid of roentgenography has shown that “as a general 
rule it can be stated that pleural effusion does not move and that mov- 
able dulness over the thorax means hydropneumothorax.” ‘There are, 
however, some exceptions. Soon after tapping a chest it may be 
observed. But here again it has been my impression that some air had 
entered the pleural cavity during the operation, while in many cases 
the lung does not completely expand soon after the fluid is withdrawn. 
Dunham quotes William 8. Thayer to the effect that pleural effusions 
move when there is an old emphysema of the lung above it; and Roger 
Morris teaches that transudates, such as are observed in cardiac and 
renal diseases, will move. However, I agree with Dunham who found 
in more than 100 cases of pleural effusion associated with tuberculosis 
of the lungs, 1t could be demonstrated by the use of the roentgen rays 
that the fluid does not move as much as half aninch. Thisis, in fact, 
of immense diagnostic and prognostic importance, because if we find 
shifting of the dulness we are to conclude that we deal with a hydro- 
pneumothorax, or perhaps with a mediastinal neoplasm in which the 
prognosis is much graver than in primary tuberculous pleurisy, or in 
simple effusions during the course of phthisis. 

Another sign of fluid in the pleura is a triangular area of dulness 
elicited near the spine on the unaffected side of the chest, ‘“ Grocco’s 
triangle.” In his first communication on the subject, Grocco? described 
it thus: 

“Paravertebral triangle of the side opposite that of the pleural 
effusion. When, with a pleural effusion of sufficient size, one percusses 
from above downward, along the spinous processes of the vertebre, 
with the patient in the sitting posture, there appears, at the level of 
the fluid, a dulness which, relative at first, becomes absolute as one 
passes downward, in association with a progressively increasing sense 
of resistance. In like manner, by percussing downward on the healthy 
side, along lines parallel to the spinous processes, there is noted, 
opposite the dulness in the median line, a paravertebral area of deficient 
resonance, of triangular shape. One side of this dull area is represented 
by the line of the spinous processes; another, by the lower border of 


1 Tr. Nat. Assn. Study and Prevent. of Tuberc., 1917, 13, 181. 
2 Riv. critica di clin. med., 1902, 3, 274; Lavori di congres. di med. int. (1902), Roma, 
1903, p. 190, 


494 TUBERCULOSIS OF THE PLEURA 


the area of thoracic resonance of a short distance, which varies in 
length from two to three or more centimeters; the outer side is repre- 
sented by a line which, starting from the base, rises obliquely to unite 
at an acute angle with the median line at about the upper limit of 
dulness. In a right-sided effusion, other things being equal, the 
paravertebral triangle has seemed to me more marked.” 

This triangle is found in nearly all cases of pleural effusion, and in 
rare cases of pneumonia, hydro- and pyopneumothorax, and cancer 
of the lung. It disappears when the patient reclines on the affected 
side. 

Auscultation shows that the friction sound, which was audible 
earlier in the disease, has disappeared. ‘The breath sounds are either 
feeble or completely absent in copious effusions. In cases which are 
followed from day to day, it may be noted that the intensity of the 
breath sounds diminishes, and distant bronchial or tubular breathing 
makes its appearance. In cases in which the effusion fills two-thirds of 
the affected pleura cavernous breath sounds may be heard. In patients 
in whom there have been signs of active pulmonary lesions, these signs 
may remain in the lung above the upper level of the fluid; they may 
become accentuated, or disappear, when the fluid is so considerable in 
quantity as to compress the entire lung. However, compression of the 
entire lung is exceedingly rare, excepting in intrathoracic neoplasms, 
and this is of immense importance in the differentiation of the latter 
from effusions due to other causes. Bronchophony is heard in large 
effusions, and in some cases whispered pectoriloquy, both of which 
are, however, also audible in other conditions involving condensation 
of lung tissue, or thickening of the pleura, or excavation of the lung. 
In some cases typical egophony may be heard, but it is at times also 
audible in pneumonia, and even in thickened pleura. 

At times we may hear over the part of the chest filled with an effusion 
any kind of rales, or crepitation. They are usually derived from the 
catarrhal condition of the fne and medium-sized bronchi which have not 
been completely compressed by the effusion. In these cases, which 
are not very rare, the diagnosis is often very difficult, but a consider- 
ation of the other signs, especially the displacement of the mediastinum, 
decides the diagnosis. 

In almost all cases the vocal fremitus is absent over the site of the 
effusion. In very rare instances when the lung is fixed by adhesions to 
the posterior wall of the thorax, it may remain normal. But this is 
diagnostically of little value in chronic cases of tuberculosis because 
this is also observed in thickened pleura and intrathoracic neoplasms. 
The vocal fremitus may also be obliterated in cases of pulmonary 
infiltration when the supplying bronchus is plugged; but vigorous 
cough may dislodge the plug and the fremitus is again palpable. 

Displacement of Organs.—In pleurisy with effusion the mediastinum 
is displaced toward the unaffected side of the chest, provided the 
exudate is ample. In effusions into the right pleura the liver may be 


PRIMARY TUBERCULOSIS OF THE PLEURA 495 


pushed downward and felt beneath the costal arch, while in effusions 
into the left side the spleen may, at times, be felt down in the abdomen, 
and the stomach also is often displaced downward. The weight of 
the fluid is sufficient to displace these abdominal organs. It is Douglass 
Powell’s opinion that it is not the amount of fluid that is instrumental 
in displacing the heart in pleurisy with effusion. Rokitansky, Frank 
Donaldson, and others, have shown that no real pressure is exerted on 
the heart till the pleura is more than two-thirds filled. Small effusions 
may displace the heart by diminishing or abolishing the elastic retrac- 
tion of the lung in the unaffected side of the chest. 

Exploratory Puncture.—In nearly all cases these signs suffice to prove 
that there is an effusion, and its location. But this should be con- 
firmed by exploratory puncture, both for general diagnostic purposes, 
as well as with a view of ascertaining the nature of the fluid. While 
in tuberculous pleurisy, as well as in all other conditions, exploratory 
puncture is a harmless procedure, yet at times we meet with some 
trouble, such as the conversion of a pleurisy into a hydropneumothorax. 
For this reason, if the general condition of the patient is good, we may 
leave the effusion alone. But in case the temperature continues high or 
hectic for more than two weeks, there are chills and, perhaps, some 
edema of the chest wall, especially if the patient begins to lose ground 
after the appearance of the exudate, an exploratory puncture should 
be made under strict aseptic precautions. Exploratory puncture is also 
indicated in doubtful cases, when differentiation between an effusion 
and a thick pleura is aimed at. But here when we get a dry tap we are 
just as much in the dark as before. In fact, in these cases of thick 
pleura the puncture must be made very carefully. The diaphragm is 
high, owing to old adhesions in various parts of the pleura, and when the 
needle is inserted low into the chest it may penetrate the peritoneum, 
the spleen, or the liver and the result is a dry tap. Large flakes of 
fibrin, thick pus, etc., may be the cause of a dry tap. In such cases the 
needle is withdrawn and reinserted in another place, but I have known 
of many cases in which several exploratory punctures proved negative, 
while incision of the chest wall showed that there was an effusion. 

Exploratory puncture is also dangerous during the first few days 
of the appearance of the effusion. It should be avoided during the 
febrile stage, because it is liable to spread the tuberculous infection by 
producing a bacteremia. In all cases in which there is no urgency, 
puncture should be postponed till the fever abates. 

Examination of the Exudate.—The fluid withdrawn should be placed 
in a sterile tube and carefully examined. The cytology of the fluid 
has been studied by many authors, but it appears that no positive 
diagnosis as to the nature of the case—tuberculous or non-tuberculous, 
—can be made in every case by a microscopical examination of the 
sediment. Some authors, notably Widal, Wolff-Eisner, and others, 
maintain that when mononuclear lymphocytes predominate in the 
sediment of the centrifuged specimen, the effusion is of tuberculous 


496 TUBERCULOSIS OF THE PLEURA 


origin, while if polynuclear leukocytes predominate, the cause is one 
of the pyogenic microérganisms, notably streptococci. On the other 
hand, D. S. Page! maintains that while a predominance of small 
mononuclear cells is usual in tuberculous effusions, they may be found 
in effusions accompanying intrathoracic neoplasms, or even renal 
disease. Page also tound that coarsely granular eosinophilic cells 
occur in large number in non-tuberculous effusions. On the whole, I 
may state that a study of the cytology of pleural effusions has not been 
of material assistance in diagnosis. 

Of more importance is an investigation of the presence or absence of 
mixed infection; various microdrganisms should be sought, especially 
streptococci, staphylococci, pneumococci, ete. As will be shown later 
on (see p. 510), tubercle bacilli are found only exceptionally in pleural 
exudates. Sterile pus, which is not extremely rare in pronounced 
cases of phthisis with empyema, is surely of good prognostic signifi- 
cance. But in primary empyemata it is never found. It has been 
my experience that pyogenic microérganisms are found in most 
tuberculous pleurisies, owing undoubtedly to mixed infection. But 
now and then we find a case of sterile pus in tuberculous pleurisy 
and, as has already been stated, the prognosis is very good when this is 
the case, provided the pleura is not infected by repeated exploratory, 
or therapeutic punctures. Therefore the cytology of the fluid should 
be ascertained in every case. It can be accomplished very easily by 
centrifuging the fluid and making a smear of the sediment, staining it 
with Loffler’s methylene blue solution. 

Roentgenography.—)ry pleurisy cannot be recognized with the 
v-rays; it is only when the pleura is thickened, and perhaps calcified, 
that it prevents the rays from passing. Hence, acute dry pleurisy 
must be diagnosed clinically, while in the later stages, when adhesions 
form, and the membranes thicken, roentgenography is at times of great 
assistance in the differentiation of intrathoracic changes. On the 
other hand, moist pleurisy is easily recognized on the screen, or the 
roentgenogram by the deep homogeneous shadow it casts on the plate. 
Small effusions may be recognized by the fact that the diaphragm on 
the affected side moves less lively during respiration; in some cases It 1s 
completely immobilized. On the right side small effusions are not 
easily differentiated because the shadow merges with that of the liver, 
but in the left pleura they may be clearly shown on the screen or plate. 
Barjon? points out that immobilization precedes the arrival of the 
fluid and remains long after the fluid has been absorbed. It has also 
been shown by Weil’ that the mobility of the diaphragm in pleurisy 
gives Important prognostic clues. If after tapping the chest of the 
effusion the diaphragm is seen to resume its normal mobility, the 
prognosis is good; there are but slight chances that the pleural cavity 


1 Lancet, 1920, 1, 585. 
2 Radiodiagnostic des affections pleuropulmonaires, Paris, 1916, p. 35. 
3 Presse médicale, 1920, p. 113. 


PLATE X1X 


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in the left pleural cavity. upper and middle lobe of right lung. 
Extensive tuberculous changes throughout 

right lung with cavitation. 





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PRIMARY TUBERCULOSIS OF THE PLEURA 497 


will refill with fluid. Conversely, if the diaphragm remains immobile 
after the fluid has been withdrawn, fluid will in all probability reaccu- 
mulate. 

In all cases of small effusions the costophrenic angle is obliterated. 
But it is important that the examination should be made with the 
patient in the erect posture, otherwise, when the amount of fluid is 
slight, these angles may not show any decided change. 

The upper limit of fluid in the pleura is not marked by a sharp 
line of demarcation between the luminous lung tissue above, and the 
dark shadow below, as is the case in hydropneumothorax. The 
shadow cast by the fluid passes gradually from the deep opacity of the 
fluid to the transparent part above. This is due to the fact that the 
lung tissue immediately above the fluid is compressed and airless to 
a degree, and is therefore not so clear on the screen or plate as the 
portions higher up, where air enters freely. Garland’s, FEllis’s or 
Demoiseau’s lines may be made out in many cases as a convexity of 
the upper level of the fluid in the axilla. 

In most cases it will be noted that the brightness and clearness of 
the upper lobe of the lung are not so pronounced as in the opposite, 
unaffected, side. This should not lead to a hasty conclusion that there 
is a pulmonary, or perhaps a tuberculous, lesion in all such cases. 
Because the lung is compressed above the fluid, and often quite con- 
gested, it does not permit the rays to pass as freely as in the opposite, 
usually vicariously emphysematous, lung. 

Another important diagnostic point needs emphasis: In nearly all, 
even very copious, effusions due to inflammatory causes the lung may 
be seen above the upper level of the fluid. When an entire hemothorax 
is found obscured by a shadow, showing no lung tissue anywhere, a 
careful inquiry should be made into the history, symptomatology, and 
physical signs of the case with a view of determining whether the cause 
of the effusion is not malignant intrathoracic disease. 

The mediastinal organs, and also the trachea, are displaced in cases 
of pleural effusions toward the unaffected side of the chest. Even 
small effusions may be thus effective, provided the mediastinum is not 
held by adhesions. | A dense shadow in the lower part of the thorax 
with the heart drawn toward the affected side points to a thick pleura 
rather than to an effusion. But to this there are frequent exceptions, 
which are discussed elsewhere. 

Localized and encapsulated effusions are often made out with 
greater certainty with the x-rays than with physical signs. ‘Thus, 
interlobar effusions are very difficult of diagnosis, but a roentgenogram 
shows them clearly,as a rule: A denseshadow running across the chest, 
while above and below it there is seen luminous lung tissue (see Fig. 
4, Plate XIX). Similarly encapsulated effusions are shown clearly on 
the plate as dark shadows in any part of the chest (see Figs. | and 2, 
Plate XIX). 

With the aid of the x-rays we may follow the effusion, noting care- 

32 


498 TUBERCULOSIS OF THE PLEURA 


fully its amount, its tendencies to increase, or its absorption, and 
especially whether the lung shows a tendency to reéxpand after the 
effusion is absorbed. On these points, the roentgen rays are superior 
to physical diagnosis In many cases. 

Course.—In non-tuberculous pleurisy the effusion is absorbed within 
a few weeks in the majority of cases. Only exceptionally does the fluid 
remain within the chest for more than two months. In tuberculous 
pleurisy the rule is that the effusion persists for months. Moreover, 
in non-tuberculous pleurisy the fever shows a tendency to abate after 
the effusion is tapped; often even when the fluid remains within the 
chest. It is different with tuberculous pleurisy. Here, tapping does 
not render the case afebrile; at most, it reduces it one or two degrees. 
In fact, in many cases the reverse is often observed. The fever may be 
trifling, but tapping the chest brings about an elevation of the tem- 
perature. The reason is obvious. While the effusion is within the 
chest, the diseased lung and with it the tuberculous lesionis compressed; 
toxemia is thus prevented as is the case with artificial pneumothorax. 
With the removal of the fluid the lung reéxpands, and moves freely 
with respiration, permitting reactivation of the lung lesion; hence, 
fever with its concomitant clinical phenomena. 

It is for this reason that I am averse to tapping pleural effusions 
indiscriminately. I have felt that in many cases the outlook for the 
patient might have been better had the fluid been permitted to remain 
inthe chest. Of course, individualization is to be practised. When the 
dyspnea becomes threatening, or the fever is very high, the question of 
tapping is to be given consideration. 

In all cases in which, despite the mildness of the general symptoms, 
the fluid shows no tendency to absorption, tuberculosis or, more rarely, 
cancer of the lung, is the cause. 

After the fluid has been absorbed the patient with non-tuberculous 
pleurisy begins to improve in general health. His appetite returns, he 
gains in weight and strength, nae the signs in his chest may disappear 
at times without leaving any trace. In many cases some thickening 
of the pleura may be detected on physical exploration of the chest. 
But this is no indication that he has remained sick. It is different with 
tuberculous pleurisies. The effusions may persist within the chest for 
months. I have seen cases in which it persisted for more than two 
years. When it is finally absorbed, the physical signs in the chest show 
unmistakable signs of a tuberculous lesion in the apex of either side, 
while over the lower lobe, at the base, signs of thickened and adherent 
pleura may be easily discerned. In a large proportion of cases 
pleural adhesions dislocate the mediastinum toward the affected side. 
This is in contrast with the location of the mediastinum while the 
fluid was in the chest. It has been my rule to consider a thick pleura 
with dislocation of the heart toward the affected side as of tuberculous 
origin, irrespective of the constitutional symptoms presented. Still, 
it does not always mean active tuberculosis. In many cases of bron- 


PLEURISY DURING THE COURSE OF PHTHISIS 499 


chiectasis, especially on the left side, dislocation of the heart is seen. 
These cases are usually sequels of pneumonia or pleurisy of non- 
tuberculous etiology. Their number has recently increased since the 
epidemics of influenza. 

During the course of pleurisy with effusion the pulmonary apex of 
the unaffected side is to be watched for signs of a tuberculous lesion. 
Very frequently a timely diagnosis is thus made. In experimental 
tuberculosis of the pleura both sides are usually found affected, though 
the inoculation has been made only on one side, as has been shown by 
Robert C. Paterson. For this reason we may find an active tuberculous 
lesion in the lung with the unaffected pleura, though as a rule the lesion 
is in the lung in whose pleura the effusion is found. 

Of course, the sputum is to be examined for tubercle bacilli at fre- 
quent intervals during the course of the disease. 


PLEURISY DURING THE COURSE OF PHTHISIS. 


As has already been stated, during the course of phthisis, the pleura 
is implicated sooner or later in practically every case. There is hardly 
a case of active, or healed, tubercle of the lung in which pathological 
changes cannot be made out in the pleura at the necropsy. The blood 
supply of the pleura, as well as its lymphatic system, shows that 
tubercle bacilli in the lungs, or the thoracic glands, almost inevitably 
must find their way into the pleura (see p. 478). Dry adhesive pleurisy 
is the result of the extension of the tuberculous process to the pleural 
membrane, in most cases. Severe cough, tugging upon these adhesions, 
or tearing them apart, may thus produce inflammation of the pleura. 
The pleurisy in such cases is, strictly speaking, of traumatic origin. 

The most common variety of pleurisy in individuals suffering from 
chronic phthisis is the dry, adhesive form, affecting only part of the 
pleura, notably that overlying the affected lung area; the areas found 
affected in the order of their frequency being the apical, that lining the 
interlobar fissures, the diaphragmatic, and the mediastinal pleura. As 
a rule, the pleura reacts to irritants by a productive inflammation lead- 
ing to adhesions of the affected areas. At times the inflammation is of 
the exudative variety and an effusion takes place into the pleural 
cavity. This effusion may be serous, serosanguineous, or purulent; it 
may fill the entire pleural cavity, or only part of it; it may be general, 
localized, or encapsulated. 

Pleurisy Accompanying Acute Phthisis.—In the acute forms of 
pulmonary tuberculosis the pleura is usually found studded with 
tubercles. In most cases the effusion is rather small and negligible 
from the diagnostic standpoint, and in many cases it is serosanguineous. 
In rare instances the effusion is copious and may even mask the under- 
lying progressive tuberculous process in the lungs, as I have seen several 
times. The symptoms of acute miliary tuberculosis, or of acute pneu- 
monic phthisis, are clear cut; the patient is prostrated with high fever, 


500 TUBERCULOSIS OF THE PLEURA 


profuse sweats, rapid heart action, distressing dyspnea, cyanosis and 
emaciation. In the miliary cases there may be cerebral symptoms, 
while in the pneumonic cases distressing unproductive cough may be 
dominating. Severe anemia and emaciation appear early and proceed 
at a rapid pace. But physical exploration of the chest revealing an 
effusion into the pleural cavity, we are apt to be misled and consider it 
a simple case of pleurisy, and raise false hopes in the patient and his 
friends. In fact, we are justified in our favorable opinion, because it 
is extremely rare that a patient with a primary pleural effusion should 
succumb. But the fever keeps on despite tapping the pleura, and the 
severe constitutional symptoms do not abate. Indeed, instead of 
relieving the dyspnea, as is usual in many cases, tapping aggravates it. 

Within a short time signs of consolidation of one of the upper lobes 
of the lungs will be noted; the patient begins to expectorate consider- 
able quantities of mucopurulent sputum which, as a rule, contains 
tubercle bacilli. Signs of excavation soon make their appearance in 
either lung. In the acute miliary cases symptoms of meningitis may 
be the terminal phenomena. 

Pleural effusions, especially serosanguineous, characterized by high 
fever, prostration, cyanosis, tachycardia and emaciation, should be given a 
guarded prognosis. If there is a history of cough, expectoration, loss in 
weight, etc., for some weeks or months before the onset of the acute 
symptoms, the cue should be taken and a careful search should be made 
for proofs of the underlying acute pulmonary process. 


PLEURISY DURING THE COURSE OF CHRONIC PHTHISIS. 


We have already stated that many of the so-called “primary” 
pleurisies are really secondary in the full sense of the word, because the 
patients had been coughing, losing in weight, sweating, etc., for some 
time before the appearance of the pleural symptoms. But in the vast 
majority of cases of pronounced chronic phthisis there are to be dis- 
cerned symptoms and signs of pleurisy at one time or another. Pain in 
the chest during the course of tuberculosis is almost invariably due 
to pleurisy. As was already stated (see p. 292), the lung contains no 
sensory nerves and only when the pleura is implicated will the patient 
have pain in the chest. 

Dry pleurisy of this type may be localized and circumscribed in any 
part of the chest, and may be bilateral. Its most common location is 
the apex; but the base, and especially the diaphragmatic pleura, are 
affected in a large proportion of cases. Usually the fibrinous exudate 
becomes organized, and the two sheets of the pleura are glued together 
by adhesions. Often large, thick strands of adhesions are seen roent- 
genographically, or at the necropsy, running from the diaphragmatic 
pleura into the depth of the lung (Fig. 2, Plate XX). Over the apex the 
adhesions are frequently seen forming a thick fibrous shell around the 
diseased area. In cases with large excavations, the thick, adherent 


PLEURISY DURING THE COURSE OF CHRONIC PHTHISIS 501 


pleura may be the only structure left instead of the upper lobe of the 
lung. 

Symptoms of dry pleurisy may be encountered during the course of 
phthisis in any of its stages. The pain in the chest is felt in the neigh- 
borhood of the affected pleura, or may be referred (see p. 483) and then 
it is felt over the shoulder, the abdominal walls, ete. During the course 
of phthisis pains in the shoulder, which may become severe and intract- 
able, should not be pronounced “rheumatic,” but a careful search 
should be made for physical signs of diaphragmatic pleurisy. Simi- 
larly, pain in the abdomen should not be attributed to gastric ulcer, 
appendicitis, cholelithiasis, ete., but a search should be made for signs 
of diaphragmatic pleurisy. In many cases a friction sound may be 
heard over the affected part of the pleura, but in others the adventitious 
sounds emanating from the parenchymatous lesions obscure it and 
render it doubtful. 

Symptoms.—Phthisical patients have no pains so long as the pleura 
is not implicated. When they get pain in the chest, they are apt to 
attribute it to a “cold.” After a chill, or any exposure, they may feel 
a sharp, at times a lancinating, pain in the chest, aggravated by 
cough or deep breathing. ‘The temperature, if normal before, becomes 
elevated to 101° F. or 102° F. Dyspnea may be distressing owing to 
the pain during respiratory efforts. 

Inspection may be of little value in most cases, because the phthi- 
sical chest already shows lack or impairment of mobility owing to the 
parenchymatous tuberculous process; the same is true of percussion. 
Auscultation reveals a friction sound over the affected area, while the 
breath sounds are usually feeble. This friction sound is, at times, diffi- 
cult to differentiate from adventitious sounds of intrapulmonary origin. 
It is, however, sufEcient to bear in mind the following points: Intra- 
pulmonary rales are usually audible as occurring during the inspiratory 
phase of respiration, or during the second half of inspiration, while 
frictions are heard during both phases, inspiration and expiration. 
Friction sounds are audible as if coming from a point near the bell of 
the stethoscope, while intrapulmonary rales appear more distant. 
Cough will influence the character of intrapulmonary rales, usually 
accentuating, rarely abolishing them, while frictions remain the same 
even after intense respiratory efforts by cough. At times friction 
sounds will become somewhat less audible after several deep inspira- 
tions, but they never thus disappear. Pressure of the bell of the 
stethoscope against the chest wall may intensify a friction sound, 
while rales remain unaffected. A friction fremitus is occasionally 
felt; but not as frequent as some books would indicate. A somewhat 
similar sensation may be felt in some cases with dry intrapulmonary 
sounds. 

These signs are more or less easily made out when the pleural lesion 
is located in the lateral aspects of the chest, especially over the lower 
lobes of the lungs and anteriorly. But when the process affects the 


502 TUBERCULOSIS OF THE PLEURA 


pleura over the apex of the lung, over the diaphragm, of the medi- 
astinum, it may be difficult to localize the pleural lesion. Over the 
apex, friction sounds may be easily mistaken for small, moist rales, or 
crepitation, and some authors have been inclined to attribute most of 
the above-mentioned sounds, when heard over the apex, to friction 
sounds, alleging that incipient phthisis is always accompanied by 
pleurisy, and the sounds are due to frictions (see p. 8346). Deep breath- 
ing, however, will accentuate intrapulmonary sounds, while frictions 
are not thus influenced. Feeble breath sounds speak in favor of pleu- 
risy, especially when the pleura is thick. Crepitation is almost invari- 
ably accompanied by bronchovesicular or bronchial breathing. With 
feeble breath sounds large, moist, consonating rales are invariably of 
intrapulmonary origin. 

Pleural Adhesions.—Dry pleurisy in pronounced phthisical subjects 
has an important influence on the course of the underlying disease of the 
pulmonary parenchyma. In addition to the painful suffering it inflicts 
it is lable to terminate in an effusion. But this is exceptional. In 
most cases adhesions result. Very often, by limiting the motion of the 
affected parenchyma, as well as through some as yet not understood 
biochemical and immunological processes, these exudates and adhe- 
sions impede the progress of the tuberculous lesion in the lung, retard 
the progress of the disease, and improve the prognosis in general. 

In most cases the adhesions are limited to the area of the pleura 
immediately overlying the diseased part of the parenchyma of the lung. 
The diagnosis may be made by paying attention to the following points: 
On inspection the affected area of the chest is seen to move but slightly 
during respiration; the motion may be restricted, or there may be 
lagging over a limited part of the chest wall. Instead of expanding 
during inspiration, the intercostal spaces will be seen to retract during 
each filling of the chest. These inspiratory retractions are of immense 
diagnostic importance, but they are not infallible. ‘They may be seen 
in cases without adhesions—when there is airless lung tissue with a 
thick visceral pleura, and this is not rare in chronic phthisis. Very 
frequently enlarged venules may be seen on the chest wall, indicating 
interference with the circulation by compression of the venous flow at 
the affected area. Moreover, owing to the retraction of the upper part 
of the pleura and lung in apical adhesions, the supra- and infraclavicular 
fossee are deeply excavated. When the basal pleura is adherent, the 
lower part of the chest appears smaller and expands to a lesser degree 
than the opposite side. Percussion elicits an impaired note, frequently 
with a tympanitic overtone, especially when the apical pleura is 
affected. Over the base the note may be flat and, because the vocal 
fremitus is absent or defective, fluid is thought of. Friction rales are 
at times heard over the apex; feeble breath sounds are the rule. Loud, 
consonating rales and clicks of intrapulmonary origin may be so pro- 
nounced as to overshadow all other sounds. It is these adhesions 
over the apical pleura that interfere with the success of therapeutic 





PLEURISY DURING THE COURSE OF CHRONIC PHTHISIS 503 


pneumothorax in many cases. They form a thick, unyielding shell 
around the diseased apex of the lung, and do not permit it to collapse, 
or to be compressed by the air which enters the pleural cavity covering 
the lower, unaffected lobes. 

When the pleura over the lower lobe is affected by adhesions, percus- 
sion may yield a normal, or even slightly tympanitic note when it is not 
much thickened. The breath sounds are almost invariably feeble in 
the lung under an adherent pleura, and tidal percussion shows that the 
affected side does not expand as efficiently as the opposite side, and that 
the diaphragm also does not move properly. Inspiratory retractions, 
while not pathognomonic, yet they are so common in pleural adhesions 
that they should be looked for in every suspicious case. However, our 
experience with the production of therapeutic pneumothorax shows 
clearly that there are no absolutely reliable signs of pleural adhesions. 
Even roentgenography fails very frequently. In cases in which all the 
signs point to adhesions, a pneumothorax may be induced at times with 
ease; while in others, in which all the signs point in the direction of a 
pleura free from adhesions, all attempts at introducing gas fail (see 
Chapter XLIV). It seems to me that only pleural adhesions with thick 
pleura, especially a thick parietal pleura, may be diagnosed, but there 
may be strong adhesions without perceptibly thickening the pleura, 
and it isin these cases that we failfrequently. It also depends on which 
pleura is thick. If it is the visceral pleura—most frequently the one 
affected—we may find signs pointing to adhesions which, in fact, do 
not exist. When the parietal pleura is thickened, we almost invariably 
will find the adhesions by the usual methods. 

Roentgenography in the Diagnosis of Pleurisy and Adhesions. —Small 
circumscribed adhesions of the pleura are not recognized with the 
x-rays. In most cases with thick, adherent pleura over the tuberculous 
apex it is impossible to state with any degree of positiveness whether 
the pleura is thick and adherent or not, because of the abnormal 
shadows produced by the parenchymatous lesion. When extensive 
and massive, a thick pleura may be recognizable, especially when the 
membrane over the lower lobes is affected. We then note that the 
convexity of diaphragm is no more a smooth line sharply demarcating 
it from the luminous lung tissue, but that it is uneven and deformed, 
and various bands of connective tissue may be noted projecting into 
the pulmonary parenchyma. The costodiaphragmatic sinus and the 
cardiohepatic angle are either obtuse or completely obliterated (Fig. 1, 
Plate XVI). The motion of the diaphragm is restricted or abolished. 

In oldercases, with more extensive adhesions, the condition may be 
recognized at first glance on the screen or plate. The ribs in the 
affected side form a very acute angle descending from the spine, the 
intercostal spaces are narrower than those on the opposite side, the 
luminous lung area is of smaller extent, owing to pulmonary retraction, 
than on the opposite, unaffected side. The mediastinum is pulled to 
the affected side. The diaphragm is immobile and often elevated. 


504 TUBERCULOSIS OF THE PLEURA 


Because of compensatory emphysema, the luminosity of the lung in 
the unaffected side is more pronounced than would be expected. 

In many cases of extensive pleural thickening and adhesions of the 
lower part of the chest, it is difficult to differentiate this condition from 
fluid in the pleural cavity, as has been intimated above. Usually the 
v-rays clear up the diagnosis. In fluid the intercostal spaces are wider, 
the mediastinum pushed to the unaffected side, ete. But we frequently 
meet with cases in which it is very difficult, or impossible, to decide as 
to what we are dealing with, with all diagnostic means at our command. 
Even exploratory puncture, when it turns out negative, may not clear 
up the diagnosis. At times it is difficult to decide whether dulness and 
the shadow on the plate found in the lower part of the chest are due to 
a thick pleura or to a parenchymatous lesion. As a rule, when the 
percussion note is dull or flat, and the x-rays do not show a deep shadow, 
the lesion is probably pleural; conversely, when the percussion note is 
but slightly impaired, or has a tympanitic overtone, we are, in all 
probability, dealing with a parenchymatous lesion. But even to this 
there are many exceptions. 

A thickened interlobar pleura cannot be diagnosed except with the 
aid of roentgenoscopy. But it may also be missed in the roentgeno- 
gram, unless the tube is placed high, on a level with the patient’s 
head so that the rays pass through the chest at an oblique angle, from 
above downward through the whole width of the thickened interlobar 
septum, thus casting a shadow of its widest and thickest surface. 
This is best accomplished by placing the tube on a level with the 
patient’s head when viewing the chest anteriorly, and on a level 
with the sacrum when viewing the* patient at his posterior aspect. 
Its appearance can be seen on Fig. 1, Plate XX. 

At times we meet with interlobar effusions which may he easily 
recognized by their physical signs—a transverse band of dulness run- 
ning across the chest along the second and third interspace, while above 
and below the resonance is clear. This, in addition to bronchial 
and, more commonly, feeble or absent breath sounds, and whispered 
pectoriloquy, should excite suspicion of an interlobar effusion when 
there are also symptoms of pleurisy, such as pain in the chest, fever, 
cough, ete. But after all the diagnosis is made positively only with 
the aid of the a-rays. But even here an intrathoracic neoplasm is at 
times mistaken for an interlobar effusion, and vice versa. 

On the screen or the plate (Fig. 4, Plate XIX) there will be seen an 
opaque band running across the chest below the second and above the 
fourth or fifth ribs. The lung is divided into three regions: The upper 
is more or less bright, the middle, dark, and the lower again bright. 
In the fluoroscope this suspended shadow may be seen moving with the 
respiratory movements of the chest, while a neoplasm is, as a rule, 
immobile. The motion of the diaphragm is practically normal. An 
intrathoracic neoplasm may also produce such a picture on the screen, 
but it is differentiated from an interlobar effusion by the clinical history 
of the case. 


PLEURISY DURING THE COURSE OF CHRONIC PHTHISIS 505 


Pleural Effusions during the Course of Phthisis.—In most cases 
the implication of the pleura in the tuberculous process passes away 
leaving adhesions and, at times, without leaving any obvious traces 
behind. Some patients thus suffer from recurrent attacks of dry 
pleurisy, so long as the tuberculous process in the lung remains active. 
In others, effusions occur. This may be observed during any stage of 
the disease. When occurring before the recognition of the lung lesion, 
we are apt to consider it as “primary”’ pleurisy, but careful inquiry 
into the past history of the patient shows the fallacy of such an assump- 
tion (see p. 489). ‘The effusion may be serous, serof brinous, serosan- 
guineous, or purulent. When it is serous the fluid can hardly be dis- 
tinguished from that found in non-tuberculous cases. As will be shown 
later on, tubercle bacilli can only rarely be demonstrated in the exudate, 
and implantation on cultures, as well as inoculation experiments, are 
too often negative to be of real diagnostic value. In the serosanguine- 
ous exudates the chances of finding tubercle bacilli are greater than in 
purely serous, or serofibrinous fluid. 

Hemorrhagic effusions occur mainly in tuberculosis, but may also be 
encountered in cancer of the lungs or pleura, in traumatic pleurisy and 
in pleurisy affecting persons suffering from certain cachectic conditions, 
notably scurvy, in certain exanthematous diseases, as hemorrhagic 
smallpox, and, exceptionally, in persons suffering from cirrhosis of the 
liver, aneurism of the aorta, and even chronic nephritis. 

In tuberculosis of the pleura the blood is derived from the rich net- 
work of bloodvessels which are at times seen in these processes, 
especially where there is a false membrane. ‘The physical signs and the 
symptoms of serosanguineous pleurisy are not different from those 
found in cases with serous effusions. It is only by exploratory puncture 
that the diagnosis is made. Put we must guard against certain sources 
of error. While performing exploratory puncture with a thick needle 
a bloodvessel may be injured and bloody fluid is seen in the barrel of 
the syringe, though within the pleura it is clearly serous. In some of 
these cases it may be noted that the first part of the fluid entering the 
syringe is bloody, then it becomes paler, and the final part is practically 
straw-colored. Rarely the reverse is observed: The first portion is 
serous, while at the end it becomes sanguineous, evidently because the 
needle touched a bloodvessel. Moreover, after one exploratory punc- 
ture, especially after tapping the chest, when serous fluid is removed, 
a second puncture, performed some time later, may show the fluid 
sanguineous even when there is no malignant disease nor tubercle of 
the pleura. The blood is then distinctly of traumatic origin. These 
cases are responsible for the numerous instances one encounters in 
which sanguineous fluid was found in the chest and no symptoms of 
tuberculosis or cancer are subsequently observed to follow. In my 
experience sanguineous fluid is mainly found in very acute cases of 
pulmonary tuberculosis, and only exceptionally in chronic cases. 

We have thus, in most cases of bloody fiuid, to differentiate between 


506 TUBERCULOSIS OF THE PLEURA 


cancer and tubercle. When due to malignancy, the history will show a 
slow onset, with little or no rise in the temperature. In some cases 
there may be found a relatively large number of coarsely granular 
eosinophile cells or corpuscles in the aspirated bloody fluid. In tuber- 
culous pleurisy with effusion the history points to an old tuberculous 
process, and there is marked pyrexia, excepting in the rare cases of 
latent effusions. Microscopical examination of the fluid shows a high 
lymphocyte count, in addition to the abundance of red blood corpuscles. 
But, as was already stated, the cytology of the fluid is not reliable 
diagnostically. 

Hemorrhagic effusion occurring during the course of phthisis may 
remain within the pleura for a long time. I have seen cases in which 
it remained for longer than two years. In rare instances tapping 
once or twice will free the pleural cavity of the fluid, but in the vast 
majority the exudate reaccumulates. In rare cases the pressure effects 
—dyspnea, cyanosis, edema of the extremities, etc.—are instrumental 
in bringing about a fatal issue; in others, the tuberculous lesion in the 
lung, or some other complication sooner or later relieves the patient of 
his earthly sufferings. 

Purulent effusions are comparatively infrequent during the course 
of phthisis. Whenever they occur I am suspicious that a latent 
pneumothorax has existed; and pneumothorax is frequently overlooked. 
I have recently paid special attention to this point, and in the majority 
of cases of empyema in phthisical subjects I have been able to discover 
roentgenographic evidence of an air pouch above the level of the fluid. 
{mpyemata are thus due to rupture of the visceral pleura at some point, 
be the loss of continuity ever so minute, and the entry of air, as well 
as secretions from the diseased lung into the pleural cavity. On 
the other hand, it is possible that empyema may occur in phthisical 
individuals without rupture of the pleura; the cases in which the 
pus is practically sterile testify to this. Similarly, during epidemics 
of acute respiratory infections tuberculous patients are often affected 
and empyema at times follows. I have seen several cases of encapsu- 
lated empyema in phthisical subjects following intercurrent influenza; 
one following an operation on the tonsils. The etiological agent in 
these cases is usually one of the various strains of pneumococci or 
streptococci. 

Symptoms.— The onset of pleurisy with effusions may be abrupt, as 
in primary cases. The patient has been getting along with his tuber- 
culosis quite well, or has been improving, when he 1s seized with pain in 
the chest, dyspnea, and cough. In other cases pains in the chest have 
been repeatedly felt by the patient, and recurrent dry pleurisy has 
been diagnosticated. But now there is noted an increase in the 
dyspnea, while coincidentally the pain in the chest disappeared. We 
also meet with patients who give no history of any extraordinary 
symptoms, but an examination of the chest reveals an effusion. ‘These 
latent pleurisies are not very rare in phthisical subjects. Fever is the 


PROGNOSIS IN TUBERCULOUS PLEURISY 507 


rule, but during the course of active phthisis this cannot guide us 
because of its almost invariable presence in these patients. In afebrile 
tuberculous patients there is noted an elevation in the temperature 
with the arrival of fluid in the chest. 

The effusion in the pleural cavity is easily recognized by the physical 
signs, and exploratory puncture which have already been detailed above 
(see p. 490). But in phthisical patients localized effusions are very 
frequent, because old adhesions limit the size of the exudate. In 
addition to the interlobar exudates which have already been mentioned 
(see p. 497) there may be localized effusions in any part of the pleural 
cavity, most commonly in the pleura lining the lower lobes. (See 
Fig. 1, Plate XIX.) In these cases exploratory punctures are to be 
made with circumspection. The site of the exudate should be clearly 
delimited before the needle is inserted, and the x-rays should be used 
freely. 

Serous and serofibrinous exudates are apt to remain a long time in the 
chest of tuberculous patients, though we often meet with cases in which 
the fluid is absorbed within a few weeks. Purulent exudates, on the 
other hand, remain indefinitely, though I have seen several cases in 
which the pus broke through a bronchus and was expectorated, the 
patient improving. But it is to be emphasized that this is merely a 
possibility. In most cases the fever keeps at a high level, is often 
hectic, characterized by frequent chills, severe emaciation, amyloid 
degeneration of the liver, spleen, kidneys, intestines, etc., and the 
patient finally succumbs to exhaustion. 

The onset of purulent effusions in tuberculous subjects may also be 
very insidious. ‘The patient has felt quite well, but of late has begun 
to lose ground; has had chills, hectic fever, nightsweats, dyspnea, etc. 
In some patients under my observation the fever was slight, there were 
no pains in the chest, and the cough was mild. But they had been 
losing in weight and strength. An examination of the chest reveals the 
presence of an effusion which, because of the mildness of the general 
symptom, is thought to be serous. But an exploratory puncture 
shows the presence of pus in the pleura. Considering the difference 
in the prognosis and treatment of serous as compared with purulent 
effusions, it is clear that in every case the nature of the fluid should 
be ascertained by exploratory puncture—the only way in which we 
may inform ourselves as to the character of a pleural effusion. In 
the majority of cases of empyema careful inquiry elicits a history 
strongly suggestive of a latent pneumothorax. In these cases the 
condition is, in fact, that of pyopneumothorax. 


PROGNOSIS IN TUBERCULOUS PLEURISY. 


As is well known, the immediate outlook in tuberculous pleurisy is 
very bright in nearly all cases. It is the ultimate outlook which is of 
importance. ‘The problems are: Will the patient, recovering from an 


508 TUBERCULOSIS OF THE PLEURA 


attack of pleurisy, sooner or later develop active pulmonary tuber- 
culosis? If he does, will the tuberculous process be of a progressive and 
dangerous type, or will it run a slow benign course? The seriousness 
of these prognostic problems is realized by every physician whenever 
he has a case of pleurisy under his care. The entire future of his patient 
depends on this ultimate prognosis of pleurisy. 

Prognosis in Primary Pleurisy.—In dry pleurisy the immediate 
outlook is almost invariably good. Within a few days, at most two 
weeks, the fever, cough, dyspnea, etc., abate, the pain diminishes in 
intensity and finally disappears, and the patient may be considered well. 
In many cases the friction sound is audible in the chest for a long time; 
I have found it in patients many months after an acute attack, but 
usually it disappears within several weeks. ‘The pains in the chest 
at times remain indefinitely; they are apt to appear during sudden 
changes in the weather, but are usually not severe enough to disable 
the patient. 

In rare cases of dry pleurisy in young persons strong and dense 
adhesions of the pleural sheets are formed, and deformities of the chest 
may result, localized retractions of the chest wall may be noted, dis- 
placement of the mediastinal organs may occur, and dyspnea may 
torture the patient, especially in left-sided interlobar pleurisy. In 
others, with basal dry pleurisy, the diaphragm remains elevated and 
more or less immobilized, and some local bronchiectasis remains per- 
manently. The result is that the patient keeps on coughing and 
expectorating for many years, perhaps for life. The prognosis is that 
of bronchiectasis, but the patient is likely to be told by some physicians 
that he is tuberculous with a basal lesion. Many of these patients are 
sent to sanatoriums during each exacerbation of the cough, expectora- 
tion, ete. In others, an acute attack simulates pneumonia. Many 
state that they had had several attacks of ‘“ pneumonia,” which, in 
fact, were acute exacerbations of the bronchiectasis. 

Dry pleurisy is likely to recur. One who has had one attack, as a 
rule, suffers from repeated attacks at irregular intervals. In these cases 
the pleura remains thickened, the mediastinum displaced, and bron- 
chiectasis develops in any part of the lung, most commonly the base. 
In others, the patient recovers from the first few attacks, but finally 
develops pulmonary tuberculosis. Recurrent attacks of dry pleurisy 
are therefore to be considered as a sure sign of tuberculosis, and treated 
as such. Especially is this true of apical pleurisy. 

Prognosis in Pleurisy with Effusion.—A pleural effusion is usually 
preceded by an attack of “dry” pleurisy. In fact, in all cases of dry 
pleurisy our immediate prognosis is to be guarded; we should wait 
some days, watchful for the appearance of fluid. When an exudate in 
the pleura is made out, the prognosis is not markedly aggravated. 
Death of a patient with a pleural effusion is extremely rare, especially 
now when, by tapping, we can avoid accidents and menacing symptoms 
due to overfilling of the pleura by the fluid. 


PROGNOSIS IN TUBERCULOUS PLEURISY 509 


Usually small or moderate-sized effusions are absorbed within a few 
weeks and the patient recovers. In many cases, fully four-fifths, the 
disappearance of the fluid leaves the patient in excellent condition; he 
soon regains his lost weight and strength, and an examination of his 
chest several months later may not show any traces of the disease which 
he passed through. In a large proportion of cases pleural thickening 
and adhesions remain. In some, bronchiectatic conditions remain 
indefinitely, manifesting themselves by periodical attacks of fever, 
cough, and expectoration, which may be influenced by the posture of 
the patient. In still others, the adhesions and sclerosis are instrumental 
in producing displacement of the heart, and dyspnea is a permanent 
feature which keeps them troubled for life. 

But the fluid may not be absorbed so soon. It may remain in the 
chest for many months. I have seen cases in which the fluid was not 
absorbed for over two years; to remain within the pleural cavity 
for two or three months is a common observation. In these cases 
tapping is of little or no avail; within a few days the fluid reaccumu- 
lates and the symptoms of intrathoracic pressure reappear. As a rule, 
when the fluid has been in the chest for a long time the fever abates; 
rarely we find a chest full of fluid in a patient with a normal tempera- 
ture. He only coughs, and is more or less short-winded. In some of 
these the tapping may result in a return of the fever, cough, etc., to 
be ameliorated, or disappear when the exudate reaccumulates. 

Of course, when a serofibrinous exudate becomes purulent from any 
cause, which happens but rarely, the prognosis is much aggravated. If 
the patient has an active tuberculous lesion in the lung, the prognosis 
is very grave indeed. Recovery is exceptional. 

I have seen one case in which a serofibrinous effusion broke through 
a bronchus, overfilled the lung, and nearly suffocated the patient. It 
is noteworthy that no infection of the pleura took place. The patient 
recovered after expectorating the fluid from his chest. 

At times we observe that tuberculous pleurisy with effusion spreads 
to other serous membranes—the pericardium, the peritoneum, and 
finally to the meninges. Some authors hold that many cases of poly- 
serositis are of tuberculous origin. A comparatively large proportion 
of patients show, as one of the terminal phenomena, symptoms and 
signs of tuberculous peritonitis with ascites; meningitis also occurs in 
rare instances. In a recent study of this subject, P. Ameuille! has 
suggested that in such cases the infective agent may be a strain of 
tubercle bacilli which has special affinity for serous membranes. But 
this requires further proof. 

There remains yet to be mentioned that in very rare instances sudden 
death terminates a case of pleural effusion. The patient, without any 
premonitory symptoms, perceives agonizing pain in the pectoral region, 
severe dyspnea, becomes cyanosed, and dies. The causes which have 


1 Am. de méd., 1917, 4, 55. 


510 TUBERCULOSIS OF THE PLEURA 


been considered as operative in these cases are: inking of the vena 
cava in left-sided effusions; pressure on the right auricle in right-sided 
effusions; embolism of the pulmonary veins, or the brain, the result 
of thrombosis in the pulmonary vessels. But in some cases none of 
these, and other suggested factors, explained the sudden death. In 
extremely rare instances tapping, or even simple exploratory puncture, 
is followed by sudden death. 

Are All Pleurisies Tuberculous?—The most important prognostic 
problem in these cases is whether the patient, after recovering from his 
pleurisy, will develop pulmonary tuberculosis, and if so, what effect 
will the pleural lesion have on the immediate and ultimate outlook for 
recovery. Experience has taught that a large proportion of patients 
with pleurisy ultimately develop phthisis. But we also know many 
who have remained alive and well for many years, or for natural life. 
For these reasons physicians warn their patients with pleurisy that 
it is not enough to treat the primary disease, but that it is absolutely 
imperative to take into consideration their chances of becoming 
phthisical. I know of many persons suffering because this possibility 
has been imparted to them by their physicians; they feel as if the sword 
of Damocles is hanging over their heads. 

It is therefore important to be able to single out the patients who are 
likely to become tuberculous ultimately, and those who are not. This 
we are not able to do in every instance, but there are indications which 
clearly show us the way in a large proportion of cases. The tuberculous 
nature of pleurisy may be determined by the following considerations: 

1. Tubercle bacilli may be found in the exudate removed with an 
aspirating syringe, or by tapping. 

2. The symptoms presented by the patient during the pleural 
disease, as well as soon after recovery. 

Tubercle Bacilli in the Pleural Exudate.—Tubercle bacilli are only 
rarely demonstrated microscopically in pleural exudates. Even in 
cases of active and progressive phthisis, the fluid is at times sterile, 
and in many cases in which micro6rganisms are found, they are usually 
the germs of pneumococci, staphylococci, streptococci, ete. Thus, 
Ehrlich found tubercle bacilli in pleural exudates only in 2 out of 
22 cases; Longa and Pensunti, in 1 out of 22; Jakowski in 1 out of 32; 
Fernet, in 3 out of 20; Thue, in 1 out of 30; Weber, in 1 out of 23; 
Landouzy and Queryat found them only once in their extensive 
experience. Netter,! collating these figures, shows that in a total of 
415 cases of serofibrinous pleurisy he found an average of 2 per cent in 
which tubercle bacilli could be demonstrated in the exudate micro- 
scopically. In my own cases it is extremely rare to find them. 

But it appears that the negative outcome of microscopic examina- 
tion of the exudate does not exclude the possibility of tuberculosis as a 
cause of the pleurisy. The fact that in cases with pronounced and 


t Thése de Paris, 1883; Bull. soc. de méd. des hép., 1891, p. 176. 


PROGNOSIS IN TUBERCULOUS PLEURISY 511 


advanced tuberculous lesions in the lungs no bacilli are found in the 
fluid, shows that there are some factors which either destroy the bacilli 
within the fluid, or interfere with their staining proclivities. Even 
though it has been my impression that many pleural effusions compli- 
cating pulmonary tuberculosis are caused by pyogenic microorganisms, 
or pneumococci, as is attested during epidemics occurring in hospitals 
for consumptives, as for instance influenza, yet a larger proportion 
than 2 per cent is undoubtedly due primarily to tubercle bacilli. 

Attempts at culturing the fluid on proper media have also failed to 
show the presence of tubercle bacilli in the majority of specimens 
examined. Similar unsatisfactory results have been obtained by 
inoculation experiments; only 10 to 20 per cent of the pleural exudates 
inoculated into animals have proved positive, as can be seen from 
the extensive statistics gathered by Chantemesse and Courcoux.! 
With improved methods, the proportion of positive results has not 
been materially increased. It has namely been found that when a large 
quantity of the aspirated exudate is injected into a guinea-pig, it is 
more likely that the animal should become tuberculous than when a 
small quantity is injected. But even with the injection of 30 ce of 
the fluid, or its centrifuged sediment, the results more often turn out 
negative than positive. 

Only recently we have been gleaning some light on this intensely 
interesting, and also very practical, problem. In experimental tuber- 
culous pleurisy with effusion, tubercle bacilli are only rarely dis- 
covered. Robert C. Paterson? found that about two hours after 
inoculating the pleura of a guinea-pig very few, or no bacilli, either 
phagocyted or free, could be discovered in the effusion. He found, 
however, that these same effusions were virulent for, and actually 
infected, normal guinea-pigs in every case when inoculated subcuta- 
neously. The problem then arises: What becomes of the baccilli in the 
effusion? It seems that in other serous membranes the bacilli also 
disappear. ‘Thus, it is very rare that tubercle bacilli are found in the 
ascitic fluid in peritoneal tuberculosis, and in cerebrospinal fluid in 
tuberculous meningitis. Rist, Roland, and Kindberg* found most of 
their peritoneal inoculation experiments turned out negative, while 
Manwaring and Bronfenbrenner* observed that the bacilli disappeared 
from the peritoneal exudates in sensitized animals. The exudate of 
serous membranes is thus apparently bactericidal. 

_ It has also been suggested that the bacilli are too few in number to 
be found with ease. in the fluid microscopically; that those which are 
present are enmeshed in flakes of fibrin. For this reason, large quanti- 
ties of the fluid, or better of the centrifuged sediment, may produce 
infection after inoculation, while small quantities fail. 


Les pleuresies tuberculeuses, Paris, 1913, p. 12, 
Am. Rev. Tuberc., 1917, 1, 353. 

Ann. de méd.; 1914, 1, 312, 375. 

Jour. Exper. Med,, 1913, 18, 601. 


- on 


012 TUBERCULOSIS OF THE PLEURA 


But after all, it seems that serous surfaces, excepting that of the 
meninges, react very favorably to infections, particularly with tubercle 
bacilli. Thus, tuberculous joints show strong tendencies to heal; so 
does the peritoneum. The same is true of the pleura. Most tuber- 
culous infections of that serous membrane lead but to dry pleurisy, 
or to small, insignificant effusions which are spontaneously and often 
quickly absorbed. Even in cases in which the entire pleura is involved 
in the process, the prognosis is good in nearly all cases, as was already 
shown (see p. 508). For this reason some authors have been inclined 
to attribute all the so-called primary pleurisies to an attenuated strain 
of tubercle bacilli. It is, however, the opinion of other writers, notably 
Koniger, that the attenuation in the virulence is due to the action of 
the exudate produced by the reacting pleura. Whether this is due 
especially to active antigens or antibodies, or to the very strong 
capacity of the pleura to absorb foreign material, cannot be stated 
with any degree of exactitude at present. This is a point which 
deserves further careful investigation. 

On the whole, it may be stated that irrespective of the cause, absence 
of tubercle bacilli from pleural exudates, as indicated by macroscopic 
examination or inoculation eaperiments, by no means shows that the 
lesion in the pleura vs of a non-tuberculous character. ‘This is of immense 
clinical importance for obvious reasons. 

Clinical Facts about the Tuberculous Origin of Pleurisy.— lor more 
than a century physicians have suspected that most of the inflam- 
matory processes in the pleura, when not due to another obvious cause, 
such as an intrathoracic neoplasm, or to cardiac or renal disease, are 
of tuberculous origin. Stoll, in the latter half of the eighteenth century, 
already considered latent pleurisy as tuberculous. Bayle said that 
‘“pleurisy is really not a cause, but an effect of tuberculosis.”’ Laennec 
was very emphatic when referring to the tuberculous nature of pleurisy. 
“Tt is absurd,” he said, ‘to believe that tuberculosis may terminate in 
pleurisy; the facts of pathological anatomy show that in the vast 
majority of cases tuberculosis may be latent for a certain time and 
‘ause no deviation from normal health, while in other cases pleurisy 
is but the first manifestation, often really the effect, of the presence of 
tubercle which existed within the body for some time.”’ 

Modern clinicians are inclined to the same view. In this country 
the first to collect a series of cases which were under observation 
for a long period of time was Vincent Y. Bowditch! of Boston, who found 
that out of 90 cases of acute pleurisy which had been observed by his 
father and followed up by himself between 1849 and 1879, 32 died of, 
or had, phthisis. George G. Sears? collected the following figures from 
the literature: Of 451 cases of pleurisy, 176, or about 39 per cent, 
subsequently developed phthisis or other well-marked tuberculous 


1 Tr. Am. Climatol. Assn., 1889, 6, 1. 
2 Boston Med. and Surg. Jour., 1892, 126, 192. 


PROGNOSIS IN TUBERCULOUS PLEURISY 513 


affections. Barr! found that out of 57 cases of pleurisy between 1880 
and 1884, 21 had already died of some form of tuberculosis, mainly 
pulmonary phthisis, at the time his report was made (1890). Couston 
and Dubrull,? from army experience, say that all soldiers who have 
suffered from pleurisy are no longer fit for military duty, and that a 
majority die later from tuberculosis. William Osler? reports that 
among 86 cases in his wards in which the after-histories were studied 
by Dr. Hamman, 34.8 per cent became tuberculous and died. In his 
Shattuck lecture’ he reports that he had carefully analyzed the post- 
mortem records of his ward cases in which pleurisy—fibrinous, sero- 
fibrinous, hemorrhagic, or purulent—was found and the result was 
that 32 were definitely tuberculous. The after-histories of 130 cases of 
primary pleurisy with effusion reported by Hedges® showed that at 
least 40 per cent died from or had tuberculosis within six years. 

The most extensive series of cases carefully analyzed were reported 
by Allard and Késter.6 Allard deals with 200 cases of idiopathic 
pleurisy treated from 1881 to 1893, their subsequent fate having 
been investigated in 1900. Késter deals with 371 cases of idiopathic 
pleurisy, and 62 of specific pleurisy, treated from 1894 to 1908, and 
reported in 1910. They also made an analysis of 2123 cases of pul- 
monary tuberculosis as to the frequency of pleurisy in their past history. 
The two series were compiled along the same lines, but independently 
of each other. In the first series, representing 180 cases of serous and 
20 of dry pleurisy, it was found that sixteen to twenty-eight vears later 
87 patients were alive and well; 28 were tuberculous, 61 had died of 
tuberculosis and 24 had died from other causes. In the second series, 
representing 334 cases of serous, and 37 of dry pleurisy, it was found 
that two to sixteen years later 164 were alive and well, 118 were 
tuberculous, 62 had died of tuberculosis, and 27 had died from other 
causes. ‘Taking the two series together, the writers find that idio- 
pathic serous pleurisy is followed sooner or later by pulmonary tuber- 
culosis in 47.7 per cent of cases, and that even in cases of idiopathic dry 
pleurisy the percentage is as high as 42. 

It has also been found that a rather high proportion of tuberculous 
patients have had pleurisy before the onset of their pulmonary disease. 
Thus Allard and Késter report that among 2123 cases of phthisis 650, 
or 30.6 per cent, gave a history of idiopathic pleurisy. E. A. Pierce’ 
analyzed two series of cases dating from 1905 until the time of his 
report. In the first series of 1767 cases of pulmonary tuberculosis, 614, 
or 35 per cent, gave a history of pleurisy. In the second series of 518 
cases, 52 per cent gave a history of previous pleurisy. He adds that, 





British Med. Jour., 1890, 2, 1058. 

Gaz. hebd. de méd., 1886, 23, 662. 

British Med. Jour., 1904, 2, 999. 

Tr. Massachusetts Med. Soc., 1893. 

St. Bartholomew’s Hosp. Rep., 1900, 36, 83. 
Hygeia, 1911, 73, 1105. 

Northwest Med., 1918, 16, 79. 


uo 7 Pp wo wD 


33 


514 TUBERCULOSIS OF THE PLEURA 


including simple adhesions with other marked changes, pleurisy was 
found in 74.4 per cent of 215 cases. 

Statistics like the above, indicating that from 30 to 40 per cent of 
patients suffering from pleurisy subsequently develop phthisis, or that 
from one-third to more than one-half the tuberculous patients have 
had pleurisy before the onset of the pulmonary tuberculosis, abound 
in medical literature. But it appears that not all clinicians have had 
the same experience; many report that, while pleurisy is often followed 
by phthisis, the proportion is not so high as the above statistics might 
lead us to suppose. Thus, Blakiston! reports 53 cases which had 
remained well for several years; Austin Flint speaks of 47 cases with 
but 3 possible instances of subsequent tuberculosis. Out of 21 cases 
reported by J. P. Bramwell? only 3 died of tuberculous disease. Cori- 
veaud® had but 4 deaths from this cause out of 27 cases, | of 
whom he had followed for twenty-five years and | for fifteen. 

That the menace of pleurisy, however significant, is not threatening 
every patient, is attested by the experience of physicians of long years 
in practice; they all have many patients who have had pleurisy, dry 
and with effusion, and remained well for years. To be sure, in hospital 
practice we encounter patients who have become tuberculous after 
pleurisy, but those who remain well do not come into hospitals. It is 
therefore important to bear in mind that while a large proportion of cases 
of pleurisy is due to tubercle, not all cases are, and not everyone develops 
active and progressive tuberculosis subsequent to an attack of pleurisy. 
In fact, more than three-fifths the number of patients with pleurisy pass 
through life without developing phthisis, as the statistics cited indicate. 
The reasons for this are to be sought for in the following facts: (1) 
Many cases of pleurisy are due to microdrganisms other than the 
tubercle bacillus, or altogether due to non-specific causes; (2) even 
when due to the tubercle bacillus, active pulmonary tuberculosis does 
not follow in all cases, and when it does, the outlook is not so gloomy 
as some statistics seem to show. 

Non-specific Pleurisy.—Pleurisy may be produced experimentally 
by the injection of irritants into the pleural cavity, especially turpen- 
tine. Injuries to the chest also are often instrumental in producing 
pleurisy. Fractured ribs, and the calluses which are produced while 
they heal, are, at times, responsible for pleurisy which is clinically 
recurring, producing symptoms at irregular intervals, not unlike those of 
dry pleurisy due to other causes. These may be considered aseptic 
pleurisies; though the ends of the fractured ribs, or the callus, may act 
as irritants and reduce the vitality of the pleural tissue, thus favoring 
the localization of bacteria brought there hematogenously. Still they 
cannot be considered specific. Similarly, pleurisy is very common in 
cases ot cancer of the thoracic viscera, and in certain cases of cardiac 


1 Quoted from Sears. 
2 Edinburgh Med. Jour., 1889, 2, 909. 
3 Jour. de méd. de Bordeaux, 1887-8, 17, 601. 


Or 


PROGNOSIS IN TUBERCULOUS PLEURISY dl 


and renal disease. Though they are not of an inflammatory character, 
yet they produce effusions. 

Among the pathogenic microorganisms, the tubercle bacillus is not 
alone holding the evil distinction of producing pleurisy. Thus, the 
metapneumonic pleurisies are very common, and those due to various 
strains of streptococci and staphylococci, influenza bacilli, etc., which 
at times occur in epidemics, cannot be considered tuberculous. I have 
been under the impression that the last-mentioned pathogenic agents 
are quite frequently responsible for pleurisy in tuberculous patients, 
occurring as it does occasionally almost epidemically in hospitals for 
consumptives. On the other hand, considering the wide distribution 
of tuberculosis in mankind, it is to be expected that many with dormant 
or latent tuberculous lesions should have them reactivated during or 
after attacks of pleurisy due to any cause. When judging statistics 
of this sort, this factor is to be borne in mind. 

Factors Influencing the Prognosis in Tuberculous Pleurisy.—It is 
a noteworthy fact, not appreciated to the extent it deserves, that when 
pleurisy is followed by tuberculosis, the outlook for the patient is not 
grave, asarule. Thus, it has been noted for many years that pleurisy 
complicating active tuberculosis may be ‘beneficial’; it is often 
observed to arrest the tuberculous process in the lung, and the patient 
improves temporarily, or even recovers, provided, of course, that only 
tubercle bacilli and not pyogenic organisms are responsible for the 
inflammation. At one time it was suggested that these pleurisies act 
beneficially by compressing and immobilizing the affected lung, thus 
affording it rest and an opportunity for the lesion to cicatrize, as 
we aim when inducing pneumothorax for therapeutic purposes. 
But further observations has shown that the mechanical factor is by 
no means the main one. It has been noted that in cases in which the 
effusion is shght in amount, and only short in duration, the effect on 
the lung may prove very salutary. In fact, in many cases of dry 
pleurisy followed by, or complicating, phthisis, the tuberculous process 
is mild, sluggish in its progress, and shows strong tendencies to heal. 
Thus K6niger' found among 49 cases of initial pleurisy, only 1 in whom 
the tuberculous process pursued a progressive course. Among 29 
cases of secondary pleurisy complicating active tuberculosis, the disease 
was favorably influenced in 27 cases. It is noteworthy that during 
the course of initial pleurisy, observes Ko6niger, ‘‘open”’ tuberculosis, 
with tubercle bacilli in the sputum, is extremely rare. Among 78 
cases he could find only 1 of this type, though in many, extensive 
changes in the lung could be made out, and they expectorated consider- 
able sputum. In my own experience also I recall but few cases of 
primary pleurisy in which tubercle bacilli were detected in the sputum 
microscopically. Furthermore, in patients with progressive and ex- 
tensive tuberculous lesions in the lungs, with excavations which have 


1 Ztschr. f. Tuberk., 1911,:17, 529. 


516 TUBERCULOSIS OF THE PLEURA 


rapidly formed, there is but rarely observed one who gives a history 
of pleurisy preceding the onset of phthisis. Of course, many adhesions 
may be found when these patients come to autopsy, but, as a rule, the 
pleural lesions had not manifested themselves by a reaction produc- 
ing special symptoms. Acute progressive phthisis following primary 
pleurisy 4 is eatremely rare, excepting in acute miliary tuberculosis, or in 
acute pneumonic phthisis which, in rare instances, is accompanied, or 
masked, by a pleural effusion (see p. 505). In our daily practice we 
meet with cases of chronic tuberculosis manifesting itself mainly by a 
thick pleura, in addition to-the infiltration or excavation of the apex, 
living on for many years. Many of these are told that “one lung is 
completely gone,”’ yet they live on, and may even be fairly active at 
their avocations, despite the activity of the tuberculous process in the 
lungs and pleura. Among these are the cases with dextrocardia, sinis- 
trocardia, immobility of the diaphragm, etc., all due to massive pleural 
adhesions, in whom the prognosis as regards duration of life is much 
better than in those in whom the pleura shows no signs of having been 
implicated materially in the tuberculous process. 

The reasons for the salutary influence of pleurisy on the pulmonary 
tuberculous process are not definitely known. Only rarely is the 
mechanical factor instrumental because, as was stated above, dry 
pleurisy, as well as small effusions, often act in the same manner. ‘The 
biochemical action of the exudate, or the inflammatory reaction of the 
pleura, may be the cause, as K6niger suggests, but so far we have no 
proof for this contention. At any rate, it seems to me that the salutary 
effect of pleurisy on the pulmonary process is due to the tendency it 
has to induce a productive inflammation. Fibrosis appears to be 
Nature’s weapon against the destructive action of the tubercle bacillus. 
Kaufmann! found that aseptic irritation of the pleura in dogs, e. @., 
introduction of nitrogen while creating a pneumothorax, induces a 
proliferation of connective tissue not only in the pleural sheets, but also 
in the interstitial pulmonary tissues, ete. Other pathological processes 
characterized by fibrosis also have a good influence on tuberculosis, 
as is the case with gout, interstitial nephritis, some cases of tertiary 
syphilis, chronic alcoholism, ete. (see p. 598). As to the substance 
which is effective in producing a proliferation of connective tissue during 
an attack of pleurisy; whether it is biochemical, or some specific 
antibody, we are in the dark. It is a subject which deserves further 
investigation. 

The prognosis in primary tuberculous pleurisy is thus not so gloomy 
as some would lead us to believe. The patient may be told that after 
the pleurisy has passed, his chances of developing phthisis are greater 
than in the average human being, still he is by no means invariably 
doomed. The majority pass through life without becoming phthisical. 
If he should be unfortunate and develop pulmonary tuberculosis, he 


1} Beitr, klin. d, Tuberk., 1912, 23, 57. 


PROGNOSIS IN TUBERCULOUS PLEURISY 517 


may be told that his outlook is rather favorable. In most cases the 
disease pursues a mild, slow course and tends to recovery. 

Influence of Age on the Prognosis.—The prognosis is also greatly 
influenced by the age of the patient. Pleurisy with effusion in children 
is not followed by pulmonary tuberculosis, as a rule. In some, bron- 
chiectasis remains for life, but the lesion is not tuberculous. From 
Allard and K6ster’s statistics it appears that the prognosis after idio- 
pathic pleurisy is much brighter in early than in middle life, and, while 
the subsequent incidence of tuberculosis is only 30 per cent when the 
pleurisy occurred between the ages of six and ten, it is as high as 
60.4 per cent when the pleurisy has occurred between the ages of 
thirty-one and thirty-five years. At the high age of sixty-six to seventy 
idiopathic pleurisy is also followed by tuberculosis in 40 per cent of all 
cases. It appears also that in tuberculosis following pleurisy, when it 
does occur in children, the prognosis is better than when it occurs in 
adults. The tendencies to recovery are more pronounced in children 
than in adults. 

Symptoms of Tuberculosis Following Pleurisy.—It is important to 
be able to single out the cases in which phthisis is likely to develop 
after an attack of pleurisy so as to institute timely treatment. We 
could then permit those who are unlikely to become phthisical to 
pursue their life-work without fear lest their occupation will be instru- 
mental in promoting the onset of the disease. It is unfortunate that 
while this problem confronts us very frequently we are not always able 
to give definite information to the patients during the course of the 
pleural affection. In some, the pain in the chest, the fever, the cough, 
etc., disappear within a few days and we may be deceived by the 
prompt recovery. Within a few weeks, or months, fever, cough, 
expectoration, nightsweats, emaciation, etc., make their appearance, 
and signs of phthisis are discovered in the chest. In others, as I have 
observed in rare instances, the recovery is complete and the patient 
returns to work, but several months later, without any assignable 
exciting cause, symptoms of tuberculous meningitis appear, and kill 
him promptly. In many with effusions the fluid is absorbed within a 
few weeks, but the patient keeps on ailing, coughs, expectorates, has 
mild fever and nightsweats, and remains anemic and debilitated; signs 
of a tuberculous lesion in the lung may or may not be clearly evident. 

A patient with any form of pleurisy who does not recover his general 
health and well-being soon after the fever abates, or the effusion is 
absorbed, should be considered as probably tuberculous and a careful 
search should be made for physical signs of a tuberculous lesion in one 
of the apices. It must be emphasized, however, that in these cases the 
tuberculous lung lesion is almost invariably localized in one of the 
apices. When physical examination of the chest shows signs of a thick 
pleura exclusively over the base, where the pleural friction was audible, 
or the exudate had occurred, the chances of the lesion being tuber- 
culous are remote; these lesions usually turn out to be bronchiectatic 


518 TUBERCULOSIS OF THE PLEURA 


and not tuberculous. When signs of a thick pleura, such as impaired 
resonance, feeble breath sounds and moist consonating rales found 
exclusively at the base, are due to tuberculosis, there is also to be 
made out a tuberculous lesion in the apex in nearly all cases. In doubt- 
ful cases of this sort roentgenography may be of immense value in 
localizing an apical lesion. Of course, the sputum is to be examined 
repeatedly for tubercle bacilli. 

Patients who recover promptly after an attack of pleurisy may be 
pronounced free from active tuberculosis at the time. But, as was 
already shown, they are more likely to develop phthisis in later years. 
It may be stated as a general rule that this predisposition wanes with 
the advance of time after the attack of pleurisy. Allard and Koster 
found from their extensive statistics that in the majority of cases 
which became tuberculous, to be precise in 85 per cent, the tuber- 
culous process flared up within five years after the attack of pleurisy. 
In younger individuals, however, it appears that pleurisy is followed 
by pulmonary tuberculosis much later. 

These conditions are illustrated even more drastically by the Ameri- 
can Medico-Actuarial Investigations of 1914. It was found among in- 
sured lives the incidence of deaths due to tuberculosis was as follows: 


Actual Expected 

deaths. deaths. Ratio. 
A. One attack within 2 years of application . . 228 154.8 147 
1B oe 4 “ 2 to 5 years of application 262 179.7 146 
C. a Li ocdsyar oa Oy ya 253 Pipe et 113 
DE = “more than 10 “* ‘e 528 573.7 92 


IngroupA and Bthedeathratefrom phthisis was observed to be about 
three times the normal; in C about twice the normal, and in D it was 
about normal, indicating that the danger of phthisis decreases with 
the time that passes after an attack of pleurisy. 

From these figures, as well as from daily observation, it appears that 
if the patient has completely recovered his health after an attack of 
pleurisy he should be told that while he may reéngage in his vocation, 
he must be careful in his mode of life during the ensuing five years. 

A careful inquiry should be made into the past history of the patient. 
Many with so-called primary pleurisy have, in fact, presented symp- 
toms of phthisis for months before the appearance of the pain in the 
chest or the symptoms and signs of an effusion, but they disregarded 
them, as has already been emphasized. In such cases the diagnosis 
of tuberculosis may be safely made. It is in these cases that tubercle 
bacilli are frequently found in the sputum. 

Prognosis in Secondary Pleurisy.—In pleurisy developing during 
the course of pronounced phthisis the outlook depends mainly on the 
underlying disease, on the condition of the tuberculous lungs, as well 
as on the resisting powers of the patient. In unilateral tuberculous 
lesions, which show no tendency to progression, an attack of dry pleu- 
risy may have no effect on the ultimate outlook. It is likely to torture 


PROGNOSIS IN TUBERCULOUS PLEURISY 519 


the patient by the pain in the chest and shoulder that it inflicts, and its 
likelihood to recurrence; but the prognosis as regards the duration of 
the disease may even be improved, as has already been mentioned. 
The same is true of an effusion. In some cases I observed that it has 
been the turning-point for the better when, before the onset of the 
complication, the course of the lung disease was active and pro- 
gressive. ‘The effusion may be slow in disappearing, but when it is 
finally absorbed the patient feels well, even though he remains with a 
thick pleura and with signs of adhesions producing dyspnea on exertion. 

It is different with extensive bilateral lesions. While in some cases 
we may even here note improvement, in the majority the reverse is 
true. The effusion ts likely to aggravate the cough, produce distressing 
dyspnea, and the fever rises higher. Hectic fever is not uncommon. 
At times the end comes suddenly through asystole, but in most cases 
the course is lingering. Repeated tappings are of little or no avail in 
many cases. In fact, it has been my impression that, very often, the 
prognosis is distinctly aggravated by tapping the exudate, excepting 
when the effusion is very copious and produces menacing symptoms 
through its mechanical effects. 

Prognosis in Empyema.—Empyema is one of the most dangerous 
complications of phthisis. Spontaneous absorption hardly ever occurs. 
Operations for the removal of pus are very unsatisfactory. The result 
is usually that the fever, cachexia, and amyloid degeneration of the 
viscera carry off the patient sooner or later. I have seen a few cases of 
empyema in which the pus found its way into a bronchus and was 
expectorated. The patients were “cured” of the empyema, but the 
tuberculous process proceeded on its course to a fatal termination. 

In general it may be stated that the vast majority of empyemata in 
tuberculous subjects are in truth cases of pyopneumothorax, and the 
prognosis is the same as in the latter condition (see p. 533). 

In very rare instances the pus becomes encapsulated and while 
remaining within the chest gives no more trouble. I have discovered 
such pus pockets in individuals who felt well and worked for years. 
Schweizer! reports such cases of chronic empyema lasting for twelve 
to eighteen years and not interfering with the patient’s earning capacity. 
Recently such a case was referred to me with a view of deciding 
whether there is an active tuberculous lesion in the lung. However, 
these patients show no symptoms or signs of active tuberculous lesions, 
as a rule. 

Another mode of termination of empyema remains yet to be men- 
tioned. While in rare cases repeated tapping may finally clear the 
pleura of the purulent exudate, in still rarer instances it has been 
observed that the pus is spontaneously absorbed and the patient 
remains with a thick pleura, pulmonary retraction, dilatation of the 
bronchi, and deformities of the chest and spine. In very rare instances 


1 Corr.-Bl. f. Schweizer Aerzte, 1919, 49, 385. 


520 TUBERCULOSIS OF THE PLEURA 


the abscess in the pleural cavity becomes encapsulated and the patient 
may go around for many years without considerable inconvenience. 
The pus in these cases changes in appearance, becoming milky-white, 
or ivory in color, as in chylothorax, and is in fact converted into 
cholestrin. In one case, with a history of pleurisy twelve years before 
he came under my observation, I withdrew with an exploratory syringe 
yellowish-white fluid, which, on microscopic examination, showed an 
abundance of cholesterin crystals. In another case the woman, forty- 
five years of age, had a very pronounced kyphoscoliosis, the result of an 
empyema during childhood. Finding signs suggestive of a pleural 
effusion, I inserted an exploratory needle and withdrew milky fluid 
which microscopically was found studded with cholesterin crystals. 


CHA Pah Re XX. Vt I: 


PNEUMOTHORAX. 


Tuts is the most frightful complication of pulmonary tuberculosis. 
It is of more significance than copious pulmonary hemorrhage because 
the latter only terrifies the patient, and its ultimate prognosis is usuall y 
favorable, as we have already shown, but pneumothorax is deadly, 
and the victim is justified in his apprehension that the collapse, and 
agonizing dyspnea, are indications that he is breathing his last. From 
West’s statistics it appears that 70 per cent of patients attacked by 
pneumothorax die, and in phthisis the proportion is even higher. 

The frequency of pleural adhesions in patients with pulmonary 
phthisis explains why all suffering from this disease do not develop 
pneumothorax. Eugene L. Opie,! making autopsies, found that nearly 
half of the focal tuberculous lesions are situated immediately below the 
pleural surface. It is not uncommon to find a calcified nodule immedi- 
ately below the puckered pleura and about it upon the adjacent pleura 
a group of small nodules. Fibrous adhesions usually bind together the 
adjacent pleural surfaces. It is thus clear that if there were no adhe- 
sions, pneumothorax would be the most common complication of 
pulmonary tuberculosis. 

Spontaneous Pneumothorax.—Many authors have applied this term 
to cases in which rupture of the pleura and entry of air into its ‘avity 
have occurred in an apparently healthy individual who has not known 
of any premonitory symptoms, nor of an acute onset, and who develops 
no subsequent hydrothorax or pyothorax. Indeed, I have had 
patients coming into my office complaining of breathlessness and 
an examination disclosed the presence of pulmonary collapse and air 
in the pleura. In most of these patients the air is absorbed within 
three to six weeks. In three cases under my care effusions developed, 
but they remained sterile and were absorbed spontaneously. Nikolski? 
collected from literature 66 cases of this kind and he found that 59 
recovered completely within eight weeks and 3 within four months. 
But there have been reported chronic and persistent cases. Bittorf? 
mentions a case lasting twenty-five years and Whitney‘ one of seven 
years’ duration. 

The origin of this form of pneumothorax has been discussed by many 
medical writers. The consensus of opinion appears to be that they 


1 Jour. Exper. Med., 1917, 25, 855. 

* Ueber den spontinen Pneumothorax, Inaug. Dis. Giessen, 1912. 
* Miinchen. med. Wehnschr., 1908, 55, 2274. 

4 Philadelphia Med. and Surg. Jour., 1886, 115, 397. 


522 PNEUMOTHORAX 


b 


are due to tuberculous lesions of the lungs or pleura. Hamman! 
agrees with those who hold that the commonest cause is a pleural 
adhesion of a tuberculous character tugging upon the visceral pleura 
and producing arent. The fact that no infection of the pleura occurs 
shows that the rent occurs about the adhesions and not over the seat of 
the parenchymatous lesion. Indeed, Flint, Letulle, and West have 
reported cases in which only a single subpleural tuberculous nodule was 
found to have ruptured and permitted air to enter the pleural cavity. 
That the rent need not be very large to produce this effect is evident 
from the fact that surgeons, while anesthetizing the brachial plexus 
with cocaine, have produced pneumothorax through a puncture with 
the hypodermic needle. Schepelmann and A. Vischer have reported 
such cases. Similarly, pneumothorax is in rare instances produced 
while performing paracentesis for exploratory purposes. 

While in the vast majority of cases the occurrence of this form of 
pneumothorax is an indication that there is a pulmonary tuberculous 
lesion, there are exceptions. ‘There is considerable evidence that spon- 
taneous pneumothorax may occur as a result of rupture of emphyse- 
matous blebs or bulle. Zahn,? Bach,’ and many others have described 
such cases, and they speak of pneumothorax due to pleural rupture 
without inflammation. A. Cahn‘ believes that sudden increase in the 
intrapulmonary pressure may be effective in tugging any small adhesion 
and thus lacerate the visceral sheet. Schule’ reports a case in which 
violent laughter was the exciting cause of a pneumothorax. It may 
also be caused by rupture of interstitial emphysematous blebs, the air 
entering the interstitial tissues and reaching the visceral pleura, forming 
a vesicle which ruptures. We often see this mechanism in cases in 
which therapeutic pneumothorax has been induced. During the 
late epidemic of influenza I met with a case which could only thus be 
explained. Spontaneous pneumothorax also occurs in rare instances 
in gangrene of the lung, bronchopneumonia complicating influenza, 
Glc. 

Spontaneous pneumothorax occurs more frequently in males than in 
females. Nikolski found it in 75 males to 14 females; Fussell and 
Riesman,° 45 and 10, respectively. Overexertion, cough, etc., are said 
to be the usual exciting causes, but at times no cause can be discovered. 

In most of the patients the air in the pleura is absorbed within a 
shorter or longer time, and they recover completely. In some, the 
recovery is but temporary, and within a few months or years there 
appear symptoms and signs of a pulmonary tuberculous lesion. In 
rare cases there have been observed recurrent attacks of spontaneous 
pneumothorax. Gabb, Vitvitski, Sale, Clyde L. Cummer,’ and others 
reported such cases. In one case eleven recurrent attacks were 


1 Am. Jour. Med. Sci., 1916, 151, 229. 2 Virchows Archiv. 1891, 122, 197. 
3 Brauer’s Beitrige, 1910, 18, 21. 

4 Deut. med. Wehnschr., 1917, 48, 1469. 5 Tbid., 1918, 44, 10. 

6 Am. Jour. Med. Sci., 1902, 134, 218. PAT bidwelOlopLoOmeo2. 


Cn 
i) 


TUBERCULOUS PNEUMOTHORAX 


observed. On the whole the prognosis is very good indeed. In fact, 
in 4 cases under my care, there was a history of indefinite symptoms of 
pulmonary tuberculosis for some time before the occurrence of pneumo- 
thorax. But the collapse of the lung was apparently of the kind called 
“providential” by some writers. After the air in the pleura was 
absorbed, the patient felt well. One has thus kept well for ten years. 

Tuberculous Pneumothorax.— As a complication of phthisis, pheumo- 
thorax is of graver significance than when occurring in apparently 
healthy indiv raul: The frequency of this ehmplication varies with 
the character of the clinical material. It is not very frequent in 
hospitals for advanced cases because only patients with old lesions, 
in whom pleural adhesions prevent its occurrence, are admitted. 
According to Powell, about 6 per cent of fatal cases of phthisis at the 
Brompton Hospital at London succumbed with pneumothorax; Wil- 
liams found 10 per cent, and Weil even 13 per cent. On the other hand, 
Biach, among 715 tuberculous cases, found only 0.73 per cent compli- 
cating pneumothorax; Blumberg, among 425 cases, 3.1 per cent; 
Drasche, among 26,231 cases, 1.46 per cent. At the Montefiore Hospi- 
tal it constitutes about 3 per cent of the fatal cases. 

As was just stated, these wide differences in the proportion of compli- 
cating pneumothorax are to be ascribed to the differences in the 
material. In many hospitals for consumptives we meet with cases of 
sudden death during the night. Some of these are due to sudden pro- 
fuse internal hemorrhages, but in most cases the cause is pneumothorax, 
which killed the patients before aid could be summoned. 

The lesion is more likely to occur in the left than in the right pleura. 
From a collection ot 234 cases reported by Louis, Walshe, WwW est, and 
himself, Powell finds that in 95 the rent was in the right and in 139 
in the left pleura. He attributes it to the greater frequency with 
which the left lung becomes the seat of tuberculous disease. 

Symptoms.—The onset is sudden, unexpected. ‘The patient has 
known that he is tuberculous for some time, and may have been assured 
that his prospects for ultimate recovery are good. But suddenly, 
like a thunderbolt out of a clear sky, after a fit of coughing, some slight 
exertion, or without any exciting cause at all, he is seized with a sharp 
agonizing pain in the chest, he feels as if ‘ ‘something has given way,’ 
or as if something cold is trickling down his side. He at once sits up 
in bed holding his hand fast over the affected side, gasping for breath. 
Acute distressing dyspnea, cyanosis, a small, rapid and feeble pulse, 
cold, clammy extremities and other phenomena of collapse soon make 
their appearance. The facial expression is that of profound agony, 
the eyes prominent, the lips livid, and the forehead clammy. ‘The 
respirations are frequent—fifty or more per minute, and superficial. 
The temperature, which may have been elevated for some time, 
suddenly drops to below normal and the cough, which may have been 
annoying before the accident occurred, ceases for a time; perhaps 
because of the pain the patient restrains himself. 


524 PNEUMOTHORAX 


In very acute cases the patient may expire within a few hours as a 
result of profound shock, dyspnea, and heart failure. Many of the 
cases of sudden death in phthisis are due to this cause. But in most 
cases the circulation adapts itself by degrees to the altered conditions 
of the thoracic viscera, the dyspnea is ameliorated, the temperature 
rises to above normal, and the patient feels somewhat relieved, the air- 
hunger not being so acute as at the onset, though he still breathes 
forty or more times per minute, and is still cvyanosed. Within a few 
days, usually between the third and fifteenth day, an effusion of fluid 
into the affected pleura is found, hydropneumothorax, or pyopneumo- 
thorax. 

The size of the perforation into the lung has but little influence on 
the acuity of the distress—a small opening the size of a pinhead may 
permit the entry of sufficient air into the pleura to collapse the lung 
completely and to displace the thoracic and abdominal organs just as 
well as a larger one. In fact, in some quickly fatal cases only a small 
opening, or slit, is found at autopsy, while in others, with large openings, 
little distress is seen, healing is rapid, and the patient may last for 
months. At the necropsy it is found that the opening is usually small, 
linear, slit-like, and occasionally circular, at times attaining the size 
of adime. In some cases there are two or even three perforations. 

Mechanism of Pneumothorax.— It is of clinical significance whether the 
perforation closes speedily and no more air or pus can pass into the 
pleural cavity, thus allowing absorption of the air. The symptoms, 
prognosis, and treatment depend mainly on this point. There are 
described in text-books three varieties of pneumothorax—open, closed, 
and valvular. In the open variety there is a patent opening which 
permits air to pass in and out of the pleural cavity, and the tension 
within the affected pleura is equal to that of the external air. In the 
closed variety the perforation has healed, and the air in the pleural 
cavity may be absorbed sooner or later, as is the case with induced 
therapeutic pneumothorax, with or without the development of an 
effusion which is generally serous. In the valvular variety, during 
inspiration or cough air enters freely into the pleura, but is prevented 
from coming out again during expiration by a valve or contraction 
of the slit. The result is that the tension within the pleural cavity 
becomes very high and, pushing the mediastinum to the opposite 
unaffected side, causes distressing dyspnea, cyanosis, and heart failure, 
till the patient is no longer able to cope with the situation and succumbs. 

This interpretation of pneumothorax has been questioned by West, 
Bard, C. P. Emerson, Castaigne, and others. West says: ‘All pneu- 
mothorax is at first valvular, at any rate more or less, 7. e., the air 
finds more or less difficulty on expiration. Thus the pleura becomes 
more and more full of air and the lungs more and more compressed, and 
this obviously tends to close the hole more or less completely. When 
the hole is of ordinary size, it will become patent on inspiration and thus 
admit air, but only so long as the pressure in the pleura is less than 








TUBERCULOUS PNEUMOTHORAX 020 


that of the air in the air tubes. As soon as the pressure on the two sides 
is equal no more air can enter, and the hole remains closed. If the 
edges cohere, the hole will remain permanently closed; if not, as soon 
as the pressure in the pleura is diminished, as it may be by paracentesis, 
the orifice may open again into the pleura. This is the explanation in 
many cases of the return of dyspnea after paracentesis.” 

It should also be mentioned that the acute and distressing symptoms 
observed in pneumothorax are not necessarily due to high pressure 
within the pleura. It has been stated that when the intrapleural pres- 
sure reaches 6 to 10 cm. of water, dangerous symptoms are bound to 
ensue. But that this is not a fact has been learned recently through 
experiences with therapeutic pneumothorax. Much higher pressure 
within the pleural cavity is often produced, over 20 cm. of water, 
without producing acute and menacing eee Actual measure- 
ments have shown that with a pressure of 15, 18, 25, and Bernard even 
raised its exceptionally to 35 or 45 em. of water, the only effect was 
that the mediastinum was displaced to the opposite side, but the 
circulation adapted itself, and the patient felt quite comfortable, at 
least during rest. The writer has repeatedly observed that when fluid 
appears in an artificial pneumothorax, the pressure within the pteural 
cavity rose to 25 or 30 cm. of water, yet the distressing and menacing 
dyspnea of spontaneous pneumothorax was lacking. 

The accommodative powers of the pleural cavity have been studied 
by Emerson.!. He found that the chest, by elevation of the ribs and 
descent of the diaphragm, can accommodate various quantities of fluid 
without any change of pressure. If fluid is continuously injected into 
the pleural space, the pressure, of course, must rise, but it tends to do 
so in stages or jerks, owing to attempts on the part of the chest to 
accommodate itself to the increase and so keep down the pressure. He 
ascribes this to a special reflex mechanism. 

As has been pointed out by Sir R. Douglass Powell, the displace- 
ment of the mediastinum is not necessarily due to the pressure exerted 
by the air in the pleural cavity. His manometric measurements have 
revealed no positive pressure in pneumothorax. From his investi- 
gations he is inclined to believe that the dislocation of the heart is 
due to the unopposed traction exerted by the elastic unaffected lung. 
Because they are no longer held up by the elasticity of the lung, the 
diaphragm and the abdominal viscera sink downward. 

Clinically this view is confirmed by the fact that tapping a pneumo- 
thorax is not always effective in relieving the patient for any dura- 
tion of time. In fact, better results are now obtained by, instead of 
tapping the pleura, insufflation of more gas (see p. 859). The recent 
experimental investigations of Evarts A. Graham and Richard D. Bell? 
of the Empyema Commission of the United States Army tend to con- 
firm this view of the mechanism of pneumothorax. 


1 Johns Hopkins Hosp. Rep., 1903, 2, 1. 
2 Am, Jour. Med. Sci., 1918, 156, 839. 


526 PNEUMOTHORAX 


Partial Pneumothorax.—In old chronic cases of phthisis we meet with 
partial pneumothorax in which there is a perforation into the pleural 
cavity, but owing to dense adhesions the air is only filling up a limited 
pouch, at a place where the pleural sheets are not adherent. ‘The onset 
is less acute and the symptoms of collapse are usually absent. The 
patient may have some pain in the chest, dyspnea, etc., but these 
attract little attention in a disease like phthisis in which these symp- 
toms are so frequent without the occurrence of pneumothorax. Careful 
physical examination may disclose signs of the condition, but it is 
easier to find it out with the aid of roentgenography. The writer! has 
reported cases in which roentgenography could not decide. It is often 
mistaken for a large cavity, especially when it is localized over an apex, 
but even in the lower parts of the chest it may exquisitely simulate 
pulmonary excavation. 

Latent Pneumothorax.—At times we meet in tuberculous patients 
pneumothorax without a history of an acute onset with pain, dyspnea, 
collapse, etc. In some of these cases careful inquiry elicits a history 
pointing to a subacute onset, but such symptoms are quite common 
in chronic phthisis without this complication. In one case admitted 
to the hospital we found complete collapse of the lung and we at first 
suspected an artificial pneumothorax, produced before admission, but 
it turned out to be a latent case. Several cases of this type have pre- 
sented themselves for examination at my office. No history of onset 
could be elicited, yet the pleural cavity was full of air and the lung 
collapsed. 

In chronic phthisis we also meet with cases in which there is a 
sudden onset with all the symptoms of this accident, but physical 
examination fails to reveal any of the signs. The French call it pneu- 
mcothorax muet, the mute form. In these cases the signs do appear, 
however, within a few days. In one of my cases of this character a 
roentgenographic plate showed that the air was filling the thoracic 
cavity for an inch or two along the axillary line. In others there was 
an interlobar air pouch. ‘These forms are best diagnosticated with the 
roentgen-rays. 

Double Pneumothorax.—Double pneumothorax has been met with 
in phthisis on exceedingly rare occasions. On Plate X XII1 is shown the 
roentgenogram of a case that came under the writer’s observation. It 
is Incompatible with life. But D. Hellin,? R. Staehelin,? and E. A. 
Gray‘ mention cases which lasted for days. 

Physical Signs.—'lhe affected side of the chest is larger—in the 
maximum inspiratory position; the shoulder raised, the intercostal 
spaces obliterated, tense and tender to the touch. While the number 
of respirations is fifty or more per minute, movements of the thorax 


1 Arch. Int. Med:;, 1917; 20; 739. 

2 Mitt. a. d. Grenzgeb. d. Med. u. Chir., 1907, 17, 414. 

3 Mohr and Staehelin’s Handbuch der inneren Medizin, Berlin, 1914, 2, 756. 
4 Tllinois, Med. Jour., 1919, 35, 252. 


TUBERCULOUS PNEUMOTHORAX 527 


are seen only in the unaffected side, while the affected side is fixed, 
almost immobile. In the vast majority of cases the apex beat cannot 
be seen, but when visible it is found at the left axillary line in right- 
sided pneumothorax and at the xyphoid cartilage, or even beyond 
it, in left-sided perforations. Vocal fremitus is abolished over the 
affected side. 

Instead of the dull note which was found before the accident, the 
affected side emits a hyperresonant, sometimes a tympanitic note, 
depending on the tension of the air within the pleural cavity. By 
comparison, the unaffected side appears to emit a defective or dull 
note. In cases in which the upper part of the pleura is adherent, and 
does not collapse, the apex is dull or “boxy” on percussion. When 
later fluid makes its appearance in the pleural cavity, we elicit a flat 
note over the lower part of the chest and the flatness changes its level 
withachangein the patient’s position (see Figs. 1,2, and 3, Plate X XIII). 
Shifting dulness is pathognomonic of air and fluid in the pleural cavity. 
Displacement of the thoracic and abdominal viscera can be made out 
more or less easily by percussion. In right-sided lesions the liver dul- 
ness disappears altogether, or is displaced downward, and the heart is 
shifted to the left, even as far as the axillary line; in left-sided pneumo- 
thorax the heart dulness may be completely absent, or displaced to the 
right, and the splenic dulness may also be absent. In fact, the spleen 
and the liver may be felt distinctly low in the abdomen. The displace- 
ment of the heart may be noted a few minutes after the occurrence of 
the accident. 

We may also elicit various metallic or amphoric notes on percussion, 
especially with a coin placed over the chest and tapping it with a stick 
or pencil, while listening with the naked ear or stethoscope over the 
opposite side of the chest. A thimble over the middle finger may be 
used percussing over the nail of the ring finger placed on the chest wall. 
The metallic sound heard while listening on the chest is exquisite. 
This method has the advantage that no assistance is needed to bring 
out the so-called coin, or penny sound. Biermer’s and Wintrich’s 
signs, as well as cracked-pot resonance, may be elicited in many cases. 

Auscultation shows complete absence of breath sounds over the 
affected side of the chest in cases in which the opening is small or 
closed and the lung is completely collapsed. When the upper parts of 
the pleura are adherent, the auscultatory phenomena of the original 
lung lesion are audible, but below no sounds at all are heard. But in 
most cases there are heard amphoric breath sounds at some point 
between the shoulder-blades. Exceptionally we meet with a case of 
pneumothorax in which the voice and breath sounds are audible in an 
exaggerated form all over the affected side. When the opening into 
the lung is large, permitting the passage of air from the bronchi into 
the pleural cavity, we may hear an exquisite variety of amphoric 
breathing, or metallic sounds, which are characteristic. The voice 
sounds, as well as the cough, may also have a metallic echo, 


528 PNEUMOTHORAX 


The splashing or succussion sound is audible at a distance in many 
cases, and the patients themselves are annoyed by it. Some patients 
know how to jerk their bodies to produce it to the best advantage. 
I have had patients in whom the succussion sound was the only indica- 
tion of fluid in the thorax, all other signs being absent because of the 
depression of the diaphragm, the result of the pressure exerted by the 
tension of the air inthe pleura. It is an excellent proof of the existence 
of air and fluid in the pleura. It is stated that it may be elicited in 
the stomach and colon, but I have not met with a case in which this 
vitiated a diagnosis. 

Metallic Tinkling.— A clear muscial note, heard at intervals on listen- 
ing over a hydropneumothorax, resembling a drop of water falling into 
a reverberating vessel, may be heard in some cases. At times it is 
only heard after cough. It is apparently not due to the falling of a 
drop at all, but to a rale produced in some portion of the lung which 
acquires a metallic character by reverberation or air bubbles exploding 
in the fluid. 

Diagnosis.—The diagnosis of pneumothorax has undergone quite 
some changes within recent years since we have had an opportunity 
to study this condition produced artificially in tuberculous patients 
for therapeutic purposes, and also since we employ roentgenography 
diagnostically in chest conditions. We now have explanations for 
some phenomena which were formerly obscure, and we know that 
certain signs formerly considered pathognomonic of pneumothorax, are 
not at all invariable accompaniments of the disease. 

In the usual case of pneumothorax during the course of phthisis the 
sudden onset of urgent dyspnea, pain in the chest, collapse, ete., 
coupled with physical signs of pulmonary collapse, suffice to establish 
the diagnosis. But there are many sources ot error. We may have 
pneumothorax without any of these acute symptoms, as has been 
already stated. In fact, since the a2-rays have been employed the 
number of latent and mute cases of pneumothorax has enormously 
increased. On the other hand, we meet in phthisis cases of acute 
dyspnea, pain, and even collapse not due to this accident. In several 
instances paroxysmal tachycardia in hysterical female patients has 
simulated pneumothorax to a marked degree. Especially difficult are 
the cases of localized pneumothorax, because the mediastinum is not 
displaced, and it may even be drawn to the affected side; a thickened 
pleura may obscure the tympany, and the absent, or amphoric, breath 
sounds may be otherwise interpreted. At times it is very difficult to 
differentiate a partial pneumothorax from a large pulmonary cavity, 
and before the advent of roentgenography mistakes of this kind were 
more frequently made than at present. The differentiation is usually 
of practical value, because the prognosis in cases with large excavations 
is very unfavorable, while with a localized pneumothorax it is more 
hopeful. 


PLATE XX 


Fre. 1 Icey 74 




















j 





Localized pneumothorax in upper third Localized pneumothorax in right side 
of right side. Interlobar fissure markedly of thorax. Note the thick bands of ad- 
thickened. Extensive tuberculous changes hesions running from the diaphragm and 
in upper lobe of the left lung. mediastinum. Diaphragm elevated. 

Hig. 3 Fig. 4 





“Ballooning.’’ Pneumothorax at high “Ballooning.” Pneumothorax in left 
pressure in the left pleura. Hernia of the pleura. Lung not completely collapsed. 
left pleura at the right side of the sternum. Left pleura protruding into the right side 


of the chest. 


PLATE XXII 


Fie. 1 





Dense infiltration of the upper half of 
the left lung with displacement of the 
heart to the left. Right lung emphyse- 
matous. 





Pneumothorax in right pleura extending 
in a thin layer of air from the diaphragm 
to the apex. Right lung slightly collapsed 
and presents consolidation at its lower 
third. The rest appears studded with 
cavities and calcified nodules. Lower 
half of left lung emphysematous; upper 
half nodular infiltration, especially at 
axilla. Heart and trachea displaced to 
the right, 


Ide, % 





From same patient as Fig. 1. Spon- 
taneous pneumothorax, air filling left 
pleural cavity and elas the heart 
to the right. 


Fig. 4 











Hydropneumothorax in the right pleura. 


PLATE XXII 


Fiq. 1 





Left pleura filled with air, but large 
cavity with dense walls under second and 
third interspace did not collapse. Nodular 
infiltrations throughout right lung.  Di- 
lated bronchi and enlarged glands in hilus 
region. 


Hie. 3 





Old fibroid phthisis with extensive 
involvement of the left lung and pleura. 
Spontaneous pneumothorax in right pleura. 





Complete pneumothorax in left side. 
Note the left lung compressed against the 
mediastinum which is markedly displaced 
to the right. 


Fia. 4 

















Diffuse tuberculous process all over 
both lungs, superadded on an anthracotic 
lung; marked peribronchial infiltrations 
and calcified glands along the hilus. The 
apex is infiltrated and adherent in the left 
side; below the clavicle there is a circum- 
seribed pneumothorax, which on physical 
exploration gave signs of a cavity. The 
lower half of the left pleura is thickened, 
which cannot be differentiated in the 
roentgenogram from fluid. 


PLATE XAIII 


Fig. 1 Fig. 2 





Hydropneumothorax in left pleura. Same patient as in Fig. 1, but body lean- 
Patient in erect position. ing to the right. 
Fic. 3 











Hydropneumothorax. Patient lying on Double pneumothorax. 
the side. 


Illustrating Shifting Fluid in Hydropneumothorax. 


TUBERCULOUS PNEUMOTHORAX 529 


“ven In cases with complete collapse of the lung, tympany may not 
be elicited on percussion, as we have learned lately in cases of artificial 
pneumothorax. It appears that it all depends on the tension of the 
air witbin the pleural cavity. In hydropneumothorax, tympany is 
found when there is but little fluid and considerable air; but when 
the effusion is copious we get flatness which disappears when the fluid 
is aspirated, provided the pleura i is not too thick. 

The position ot the heart is usually of assistance in deciding whether 
we deal with a large cavity or a pneumothorax: In the former it is 
displaced toward the affected side, while in the latter it is moved 
away from it. But even here there are many important exceptions, 
owing to previous pleural adhesions, ete. Roentgenography usually 
decides, but not always. | 

The signs obtained on auscultation differ very much in cases of open, 
as compared with closed pneumothorax, and in the latter cases it 
depends on whether the lung is completely or only partially collapsed. 
A closed pneumothorax ih complete collapse is mute; no breath 
sounds at all are audible, as a rule. At times we perceive some bron- 
chial breathing in the interscapular space emitted from the bronchi 
near the spine. In the open variety we usually hear amphoric breath- 
ing of an exquisite type. In many cases of phthisis, in which the pleura 
is free all over, it is adherent at its upper third, over the site of the main 
lesion, and does not collapse at that place, and we obtain the breath 
sounds and rales peculiar to the diseased lung. 

The breath sounds often audible over a completely collapsed lung 
were formerly attributed to some opening into a bronchus, allowing 
air to pass in and out of the pleura. We now know that this is not 
always the case because in artificial pneumothorax, where an opening 
into the lung is positively excluded, we often perceive the same acoustic 
phenomena. It seems that the air in the pleural cavity is capable 
of transmitting the sounds in the bronchi when in a certain condition 
of tension. More often bands of adhesions running from the collapsed 
lung toward the periphery act as conductors of the sounds originating 
in the trachea and bronchi. 

The bell sound is very frequently elicited in cases in which the effusion 
is not too thick, as in some cases of pyopneumothorax. It is easily 
elicited by placing a coin over the anterior surface of the thorax and 
percussing it with another while auscultating posteriorly or in the 
axilla. A clear, ringing, bell-like sound, sahicll is characteristic, 1s 
heard. But exceptionally it is also heard over large cavities, or 
even a dilated stomach. It is often absent in pneumothorax; but 
when heard it is of significance, showing, as it does, air and fluid in the 
pleural cavity. We may hear it only with the patient in the horizontal 
position. In some it appears only after some of the fluid has been 
aspirated. 

A positive diagnosis of pneumothorax can be made when one is 
alert and looks for it in every suspicious case. In most cases the 

34 


530 PNEUMOTHORAX 


abrupt onset of the urgent symptoms and the physical signs suffice. 
In doubtful cases the roentgen rays decide easily and speedily. 

A rare complication of pneumothorax, the spontaneous as well 
as the artificial varieties, is pneumopericardium—air entering the 
pericardial sac. We then have instead of the cardiac dulness, hyper- 
resonance or tympany, sometimes cracked-pot sound. On ausculta- 
tion we hear that the heart sounds are extraordinarily intensified, and 
a splashing sound is audible, or a succussion sound, synchronous with 
the systole. In the case observed by the author there was also a 
metallic tinkle and a friction fremitus, especially when the patient bent 
his body forward. Similar cases have been reported by Wenckebach,! 
Cowan, Harrington and Riddell, and Meyer. With the aid of 
roentgenography the diagnosis offers no difficulty. 

Roentgenography.— The x-rays have their greatest field of usefulness 
in our attempts at discerning the changes in the thoracic organs when 
the lung is collapsed by air in the pleural cavity, especially in the local- 
ized variety of pneumothorax, which formerly escaped attention in 
most instances. Complete pneumothorax is clearly seen on the fluoro- 
scopic screen or the roentgenographic plate. The affected hemothorax 
shows a very bright area, lacking in lung markings; in contrast with the 
opposite expanded lung it may be said to be brilliant. The ribs on 
the affected side are more sharply demarcated than on the opposite 
side; the costophrenic angle is clearly seen and runs rather acutely 
downward. The collapsed lung is seen lying near the mediastinum, or 
against thespinal column, as a dark band (see Figs. 1,and 2, Plate X XII). 
During respiratory efforts the collapsed lung becomes somewhat larger 
and brighter. In many cases of tuberculous pneumothorax some part 
of the lungs, especially the apex, is retained in its position by adhesions. 

The mediastinal organs are, in most instances, displaced toward the 
unaffected side; very frequently the trachea is thus displaced. In 
many cases we may note rhythmic movements of the mediastinum, 
especially the heart; during inspiration the mediastinum is moved 
toward the unaffected side. The dome of the diaphragm is lower than 
that of the opposite side; its convexity is gone, and an almost straight 
line may be made out running downward and outward. The inter- 
costal spaces are wider, and the ribs, as well as the diaphragm, move 
less during respiration than those of the unaffected side. In some there 
is complete immobility of the affected half of the thorax. In some 
cases the paradoxical phenomenon in the diaphragmatic motion, first 
described in Kienb6ck, may be noted. Instead of the normal, simul- 
taneous contraction of the two halves of the diaphragm during each 
inspiration when they descend like pistons, there is observed a dissocia- 
tion of this movement. ‘The two sides of the diaphragm behave like 
two sides of a balance: While the unaffected half descends the 
affected half rises into the thoracic cavity. 


1 Ztschr. f, klin. Med., 1910, 71, 402. 
2 Quarterly Jour. Med., 1914, 7, 165. 
3 Medical Record, 1915, 88, 991. 


LOCALIZED PNEUMOTHORAX 531 


When fluid appears in a pneumothorax it is easily discerned with the 
x-rays. Itis, however, important that the examination should be made 
with the patient in the erect posture, otherwise the fluid may spread 
out all over the chest and thus escape notice by those who have little 
experience with these cases. The fluid sinks down, and is seen as a 
deep shadow occupying the lower part of the chest, while the upper 
part, Just above the level of the fluid, is bright. It has been well com- 
pared with a bottle half-filled with ink. The line of demarcation 
between the fluid below and the air above is sharply drawn, which is 
in contrast with effusions in pleurisy in which the dark shadow of the 
fluid merges by degrees into the bright lung tissue above. Inclining 
the patient to the side will shift the level of the fluid (see Figs. 1, 2, and 
3, Plate XXIII). Insome casesshaking the patient may cause agitation 
of the fluid within the chest, showing the mechanism of succussion. 

Localized Pneumothorax.— As has already been stated, the diagnosis 
of localized pneumothorax is at times important owing to the difference 
in the outlook for the patient: The prognosis is good in many cases of 
localized pneumothorax, while it is poor in those with large pulmonary 
excavations. In our attempts at this differentiation we should bear in 
mind the following points: 

The history of the onset is most important in nearly all doubtful 
cases. A pulmonary cavity of large dimensions does not appear sud- 
denly, while signs of a localized pneumothorax appear within a few 
minutes. If we have had the patient under observation for some time, 
the sudden appearance of signs of excavation, such as tympany, 
amphoric breathing, and pectoriloquy over a circumscribed area, 
should suggest pneumothorax. In most patients we find that there has 
been a sudden change for the worse, even in such as have been doing 
quite well. A sharp, stabbing pain in one side of the chest is felt, fol- 
lowed by dyspnea, cyanosis, prostration of variable degrees, etc. But 
we meet with many cases in which the history is negative. 

While in some cases a localized pneumothorax may prove fatal within 
a short time, in most the acute symptoms abate within a few days, 
the pain disappears, the dyspnea is ameliorated, though the patient 
remains short-winded on slight exertion. 

Physical exploration of the chest shows that in localized pneumo- 
thorax the cavity is, as a rule, “dry,” no adventitious sounds are 
audible; while large excavations usually show large, moist, consonating 
rales and gurgles. A large, “dry” cavity, especially when extending to 
the axilla, should not be accepted as such without careful investigation. 
The breath sounds in pneumothorax are distinctly amphoric or metallic; 
such exquisite metallic sounds are exceedingly rare in cavities. In the 
former a metallic tinkle may be heard, which is exceedingly rare in the 
latter. In cavities bronchophony is the rule, and whispered pectorilo- 
quy is frequently absent, while in localized pneumothorax the latter is 
commonly present and is strikingly pronounced, clear, and articulate, 
usually perceived as if spoken directly into the stethoscope, a phe- 


532 PNEUMOTHORAX 


nomenon exceedingly rare in pulmonary excavations, in which only 
the spoken voice is transmitted. The whispered echo is also more 
frequently heard in pneumothorax. Moreover, in localized pneumo- 
thorax, especially the interlobar variety, whispered pectoriloquy is 
distinctly or exclusively heard high up in the axilla, which is very rare 
in cases with excavations. On inspection retraction of the chest wall 
is characteristic of large cavities, while bulging may be found, though 
rarely, in cases of localized pneumothorax. The location of the medi- 
astinal organs gives no reliable criteria as to the condition. They are 
almost invariably displaced toward the affected side in large cavities 
but the adhesions which are instrumental in localizing the pneumo- 
thorax may also keep these organs in the place they had been before 
the rent in the pleura had occurred. 

The roentgenographic findings are invaluable in most doubtful cases. 
A bright, circumscribed area, lacking in lung markings, when not 
surrounded by a thick, dark shadow, is almost pathognomonic of a 
localized pneumothorax. But at times even this is deceptive. The 
air pouch may be located anteriorly, while posteriorly adherent lung 
tissue screens it, and no bright area appears on the roentgenogram, as 
I have seen in some cases. On the other hand, the walls of the pul- 
monary cavity may not cast a shadow on the roentgenogram, and as a 
result we may find on the plate a picture clearly showing a pneumo- 
thorax, while the real lesion is a large pulmonary cavity. Such anoma- 
lous findings at necropsy have been reported by many clinicians and 
roentgenographers. The writer! has reported cases showing localized 
pneumothorax distinctly on the x-ray plate, yet the autopsy showed a 
large cavity in the lung. It seems to me that in such doubtful cases 
fluoroscopy is of more value than roentgenography. In localized 
pneumothorax we often see the mediastinum rhythmically moving 
during the respiratory act; during inspiration it is moved toward the 
affected side. This is best seen in artificial pneumothorax, after the 
first one or two fillings, when there is but a small air pouch in the pleura. 
In the spontaneous variety, when the adhesions are not dense enough 
to hold the mediastinum very fast, we may observe the same phe- 
nomenon, and this is never seen in cases of large cavities. In most 
cases it is, however, easy to differentiate on the roentgenogram between 
cavities and localized pneumothorax. In extensive disease, pulmonary 
cavities are usually multiple; they contain not only air, but also 
secretions which are not constant in quantity, changing intermittently, 
and bridges made up of connective tissue and bloodvessels. No clear, 
bright area lacking in lung markings is, as a rule, produced on the 
roentgenogram; their margins are more opaque and the pulmonary 
tissue around them is denser than in localized pneumothorax. Bearing 
these points in mind, we may differentiate the two conditions in most 
doubtful cases. In some, as we have shown, this is impossible. 


1 Arch. Int. Med., 1917, 20, 739. 


pLe, 
Oo 


LOCALIZED PNEUMOTHORAX Box 

Prognosis. —On the whole, the prognosis in spontaneous pneumo- 
thorax during the course of pulmonary tuberculosis is decidedly gloomy, 
Occurring, as it does, in patients who are already doomed because of the 
condition of the lungs, this accident but accelerates the inevitable. 
In very acute cases the patients succumb within a few days, and 90 
per cent die within a month. An open pneumothorax, permitting the 
entry of the contents of pulmonary cavities into the pleura, is almost 
invariably fatal, sooner or later. 

The writer has seen cases of hydro- and pyopneumothorax that have 
survived for years, and some in whom the fluid has been absorbed, but 
they are exceedingly rare. Most patients with pyopneumothorax that 
I have seen have succumbed within one year after the onset of this 
complication. 

Conditions are somewhat different in cases with closed pneumo- 
thorax, and also in the localized forms of this condition. They usually 
occur in patients with slight lesions and with good resisting power. 
So long as there is no communication with a tuberculous cavity, and the 
pleura is not infected, as is the case with artificial pneumothorax, the 
air in the pleura may in time be absorbed. In fact, it was these rare 
cases of collapse of the lung, and the resulting amelioration of the 
symptoms of phthisis, which suggested the idea of therapeutic pneumo- 
thorax. 


CHAPTER XXVIII. 


DIFFERENTIAL DIAGNOSIS OF PULMONARY 
TUBERCULOSIS. 


SPEAKING of the diagnosis of pulmonary tuberculosis, some assume 
that it is only important to differentiate the disease in its early or 
incipient stage, while when the lesion is more or less advanced the 
nature of the ailment is so clear that anybody, even of the laity, may 
make a diagnosis. That this is not the fact is clear when we contem- 
plate the relatively large proportion of non-tuberculous cases admitted 
to and at times kept for long periods in hospitals for advanced con- 
sumptives. Thus, J. Earle Ash! found that among the 198 autopsies 
that have been performed at the Boston Consumptives’ Hospital since 
its foundation, 23 cases, or 11.5 per cent, proved to be non-tuberculous 
in so far, at least, that no active tuberculous lesion could be discovered. 
That this is not a unique condition is shown by other figures reported 
by Ash. He inquired in other hospitals for advanced tuberculous 
patients in this country and obtained facts about 353 autopsies, 
among which 38, or 10.8 per cent, were found non-tuberculous. 
McCrae and Funk? have had similar experience: Among 1200 con- 
secutive admissions, all patients coming with a diagnosis of advanced 
pulmonary tuberculosis, 72, or 6 per cent were found to be non-tubercu- 
lous. Of 134 necropsies, 5.2 per cent were found non-tuberculous. 
Into my service at the Montefiore Hospital there are very frequently 
sent patients who had spent many months, or even years, in various 
sanatoriums and hospitals for consumptives, but a careful clinical 
study of their cases shows that they present no signs of active tubercu- 
losis in any stage or form, and other diseases are diagnosticated, at 
times confirmed by autopsy. 

The number of incipient cases of tuberculosis which, on careful 
study, prove to be non-tuberculous, is undoubtedly higher. The fact 
that sanatoriums have a large proportion of “sputum negative” 
patients, some as high as 50 per cent, testifies strongly in favor of this 
view. When we bear in mind that hardly more than 10 per cent of 
“sputum negative’ cases—in which the sputum was examined several 
times and revealed no tubercle bacilli—are actually tuberculous, it is 
clear that many other clinical conditions pass for tuberculosis 
very frequently. This was clearly demonstrated in the European 
armies, in which, at the beginning of the struggle, tens of thousands 


1 Jour. Am. Med. Assn., 1915, 64, 11. 
2 Tbid., 1919, 72, 161. 


DISEASES OF THE UPPER RESPIRATORY PASSAGES 535 


had been rejected by the draft officers and from army hospitals, 
but a careful examination showed that hardly one-third of these 
were really tuberculous. To be more exact, of 1000 men sus- 
pected of being tuberculous in the French Army, only 1.5 per cent 
proved to be actually tuberculous, according to Kindberg and Del- 
herm.! Eduard Rist? reports that in 1000 men sent back to a base 
hospital as suffering from pulmonary tuberculosis, only in 193 was the 
diagnosis confirmed by a careful study of the cases. In the rest many 
other diseases of the lungs, bronchi, and especially the rhinopharynx, 
were found. In Germany, according to Gerhardt,’ incipient tubercu- 
losis is diagnosed far more frequently than facts would warrant, both 
during peace and during war times. Many patients who spent years 
in sanatoriums were found at autopsy years later with absolutely intact 
lungs despite the error committed in finding apical lesions while admit- 
ting and keeping them in the institutions. A. Fraenkel‘ found that in 
Heidelberg only 40 per cent, in Halle, only 26 per cent (Hesse), and in 
Jena as few as 18 per cent were really tuberculous according to Frie- 
sicke. 

The sufferings inflicted on the patients, their relatives and friends 
by a diagnosis of tuberculosis, and the stigma it imposes on them, 
perhaps for life, as well as the economic loss sustained by the indi- 
vidual patient and the community, by such a diagnosis should make 
us hesitate before pronouncing a case tuberculous. But this can only 
be done when we have a clear appreciation of the pathological condi- 
tions which are likely to be mistaken for tuberculosis. In the following 
pages will be enumerated and discussed those disease conditions which, 
in the experience of the writer, are most commonly mistaken for 
phthisis. 

Diseases of the Upper Respiratory Passages.—In the author’s 
experience, the most common pathological conditions mistaken for 
tuberculosis are diseases of the upper respiratory passages. A large 
proportion of the “suspects,” as well as of the “incipient cases with 
negative sputum,” treated in tuberculosis clinics, and often admitted 
to sanatoriums where they may be kept for an indefinite time, have 
no discoverable lesions of any kind in the lungs, bronchi, or trachea. 
Their main troubles are located in some part of the throat, the tonsils, 
the pharynx, or one of the nasal sinuses. Many have been operated 
upon for these conditions one or more times. These patients often 
cough, expectorate mucopurulent material, at times streaked with 
blood, ete. During some intercurrent affection, or a subacute exacer- 
bation of the rhinopharyngeal trouble, they may have some fever, 
anorexia, lose in weight and strength, etc. Streaky sputum at this 
time is sufficient incentive for a thorough examination. If some 

1 Presse Méd., 1917, 25, 645. 
2 Jour. Am. Med. Assn., 1917, 69, 1266. 
3 Miinchen. med. Wehnschr., 1918, 66, 556. 


4 Tbid., 1916, 64, 1109. 
5 Tbid., 1917, 65, 1502. 


536 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


impaired resonance is found in one of the apices—and the right apex 
is very frequently deficient in air content in these cases—a diagnosis 
of tuberculosis is made, or at least the patient is placed in the category 
of the “suspects.” Fastidious physicians find in these cases not only 
impairment of resonance in one of the apices, but also some clicks, or 
rales provoked by cough, and, perhaps, some prolongation of the 
expiratory murmur, or even bronchovesicular breath sounds. How- 
ever, repeated examinations of the sputum fail to reveal the presence 
of tubercle bacilli. But this does not deter some physicians from 
making it a case of tuberculosis with negative sputum; some examining 
physicians for sanatoriums pronounce them tuberculous and admit 
them to institutions. 

In children these chronic rhinopharyngeal conditions, especially 
adenoids and enlarged tonsils, are even more often responsible for the 
erroneous diagnosis of tuberculosis, or of tracheobronchial adenitis, 
because they do not thrive, have mild fever, sweat at the least exertion, 
or at night when retiring to bed, ete. In fact, in many of these children 
impairment of resonance may be found in one of the interscapular 
spaces. | 

The differential diagnosis of these nasal conditions from tuberculosis 
is based on one principle which is very important to bear in mind. 
Tuberculous disease, when active, is accompanied by symptoms of tox- 
emia, particularly fever and tachycardia. Atleast the temperature and 
pulse are unstable (see pp. 217, 278). While a slight rise in the tem- 
perature may, at times, be discovered in patients with adenoids, 
hypertrophied tonsils, ete. (see p. 458), it is very uncommon. But the 
pulse-rate is hardly ever affected in these cases. The cough in rhino- 
pharyngeal disease differs markedly from that of incipient phthisis in 
most cases. The phthisical subject states that he had never coughed 
until the onset of the disease, while the patient with rhinopharyngitis 
has coughed for years, rather mildly hawking up every morning some 
tenacious sputum, at times streaked with blood, especially during an 
acute exacerbation; he has been “subject to colds.” An examination’ 
of the nose and throat usually reveals the source of the trouble— 
enlarged tonsils, adenoid vegetations in the pharynx, hypertrophied 
turbinates, chronic sinusitis, atrophic rhinitis, ete. There may also 
be found some varicosities on the posterior wall of the pharynx, tongue, 
or trachea (see p. 244) which are the source of the blood in the sputum. 

The mistake of pronouncing these patients tuberculous may be 
avoided in the vast majority of cases by adhering to the following 
guiding diagnostic principles: No patient should be pronounced sick 
with active phthisis unless there are found distinct signs of an apical 
lesion, with positive sputum, when the pulse and temperature are normal, 
when he states that he has been “subject to colds” for many years, and 
shows signs of pathological changes in the nose or throat. Only consti- 
tutional symptoms of phthisis, such as fever, tachycardia, languor, loss 
of flesh, ete., and tubercle bacilli in the sputum, justify a diagnosis 


COLLAPSE INDURATION OF THE APEX 53 


of tuberculosis when the physical signs of a lesion in the lung are lacking 
or are indefinite. It is, at times, advisable to send these patients to 
the country for a few weeks’ vacation and it will be found that they 
improve very rapidly, cease coughing, and gain in weight and strength. 

Children with enlarged tonsils or adenoids often show marked rises 
in temperature every afternoon. Some of the temperature curves of 
these little patients are not unlike those obtained in tuberculous cases. 
But we must bear in mind that while subacute and chronic disturbances 
in the throat are common in children, pulmonary tuberculosis is rare. 
In addition, children with enlarged tonsils and adenoids, with the 
lymphatic constitution, are peculiarly resistant to tuberculosis (see p. 
588). Moreover, their temperature is unstable, and liable to fluctua- 
tions not observed in adults (see p. 458). It is therefore imperative 
that these factors should be taken into consideration before pronouncing 
a child tuberculous and perhaps rob it of an education. In children of 
school age tuberculosis should be diagnosed only when there are 
definite and clear-cut signs of a lung lesion, especially when the symp- 
toms may be explained as due to evident pathological changes in the 
nose and throat. Lymphatism in children excludes tuberculosis m 
an active stage, as a rule. Tuberculous tracheobronchial adenitis, 
on the other hand, is quite common among these children, but the 
prognosis is much better than is generally appreciated (see p. 471). 

Collapse Induration of the Apex.—In many persons who have been 
troubled with nasal obstruction for years, certain changes occur, which 
give physical signs often closely simulating those of tuberculous lesions 
in the apex of the lung, especially the right. 

The symmetry of the two apices is not always perfect, nor do they 
always have the same resonance and breath sounds in most of appar- 
ently healthy people. In many the differences are so striking as to 
attract attention, and when cough, expectoration, fever, etc., occur 
for any reason, a diagnosis of tuberculosis is apt to be made based 
upon the asymmetrical findings over the upper parts of the chest. In 
persons suffering from adenoids, enlarged tonsils, or other nasal or 
pharyngeal obstruction, collapse of the parenchyma of the right apex 
is often met with; the air within the alveoli is resorbed, and the lung 
tissue becomes indurated, greatly simulating conditions in phthisical 
lesions. Krénig! was the first to describe these cases in detail, and 
after him many other writers have reported that it is one of the most 
common respiratory disorders mistaken for phthisis. Many of the 
negative sputum cases In sanatoriums belong to this class. 

It is a purely local, non-specific induration of the lung apex showing 
physical signs exquisitely simulating those of phthisis. The following 
points of differentiation may be of value: Patients with collapse 
induration have suffered from nasal obstruction since childhood, and 
generally have chronic pharyngitis, enlarged turbinated bones, ade- 


1 Deutsche Klinik, 1907, 11, 634. 


588 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


noids, or hypertrophied tonsils. They complain that they have not 
been able to breathe properly through the nose for years, have expec- 
torated considerably, suffered from dryness and itching of the throat, 
and have had a strong tendency to colds, tonsillitis, and frequent 
bronchial catarrh. The classical facies of the mouth breather is often 
observed in these patients—open mouth, enlarged and drooping lips, 
obliteration of the nasolabial fold, ete. In tuberculosis all these are 
lacking. In fact a tuberculous patient with pronounced stigmata 
of the lymphatic diathesis is exceedingly rare. The sputum shows 
distinct evidences that it is derived from the upper respiratory tract. 
It is watery, mixed with saliva, and colorless; sometimes containing 
gray or bluish globules, not unlike the kind seen in pneumokoniosis. 
Microscopically there are often found epithelial cells from the mouth, 
nose and throat, but no tubercle bacilli nor elastic tissue. 

Again it must be emphasized that the toxemia of tuberculosis is not 
observed in these cases. The pulse and temperature are normal, and 
the nutrition of the patient remains good, excepting during an acute 
exacerbation of the rhinopharyngeal conditions. The general appear- 
ance of the patient is good. Despite the fact that he has been coughing 
for many months or years, he appears well nourished and does not 
lose in weight, as is usual in active tuberculosis. He is able to keep at 
his work efficiently, and the sense of fatigue and languor characteristic 
of phthisis is lacking. 

Apical Catarrh.—Most of us have been warned against the term 
apical catarrh of a non-tuberculous nature as something which does 
not exist and should be banished from medical terminology. But it 
appears that during recent years the profession is again acknowledging 
that there is often to be seen a catarrhal condition of one or both apices 
which is not caused by tubercle bacilli. This is especially to be observed 
in persons who have symptoms and signs of pulmonary emphysema, 
and those working at dusty trades. They often show all kinds of rales 
when their apices are auscultated, particularly after vigorous cough 
due to local bronchitis or tracheitis and to atelectasis. There may be 
some hoarseness during the morning hours, due to the accumulation 
of secretions upon the vocal cords, which disappears during the day. 
The difficulty of differentiating these cases from tuberculosis, especially 
fibroid phthisis, are often immense. In my wards at the Montefiore 
Hospital we must, at times, keep these patients for weeks, and examine 
the sputum many times before we can make up our minds as to the true 
nature of the trouble. In nearly all cases there is to be observed 
impaired resonance over one or both apices, but it is to be distinguished 
from dulness due to tuberculosis by the fact that there is no apical 
retraction—the resonance above the clavicle usually remains clear, 
while below the clavicle dulness is elicited as far as the second or third 
interspace. This is a sign which should always be looked for. Many 
of these patients are really sufferers from the emphysematous form of 
fibroid phthisis. But at this stage no special and costly treatment is 
indicated. It occurs most commonly in persons over forty. 


CHRONIC PNEUMONIC PROCESSES 539 


The symptoms of tuberculous toxemia are also lacking; there is no 
elevation of the temperature nor acceleration of the pulse, excepting 
in the later stages of the pulmonary emphysema, when there are signs 
of dilatation of the right heart. The blood-pressure is often high, while 
in phthisis it is low. 

In younger individuals apical catarrh often remains after epidemic 
influenza. Here the onset suggests an acute exacerbation of a tubercu- 
lous process, and the physical signs, combined with the cardinal symp- 
toms, cough, debility, anemia, etc., are very often misleading. But 
no tubercle bacilli can be discovered, while the constitutional symptoms, 
fever, tachycardia, etc., are lacking; in fact, after an attack of true 
influenza the pulse is, as a rule, slow. The prompt recovery of the 
general health within a few weeks proves that the catarrh is of non- 
tuberculous origin. Here again we may get a clue by noting that there 
are no signs of apical retraction, the resonance above the clavicle is 
normal, and Krénig’s field is not contracted in catarrh, while in tuber- 
culosis it usually is. In some cases prolonged observation is required 
before a positive diagnosis can be made. 

Chronic Pneumonic Processes.—Cases which simulate tuberculosis 
to a degree as to prove baffling are those caused by pulmonary infec- 
tion with various cocci. In some only observation for many weeks 
will clear up the diagnosis. The first to make a careful study of these 
pulmonary infections was Finkler,! who found that they are mainly 
due to various types of streptococci. Recently many others have 
published extensive clinical and bacteriological studies and have shed 
considerable light on some of the obscure phases of this condition. 
From the studied of David Riesman,? William Charles White,’ Louis 
Hamman and S. Wolman,‘ A. H. Garvin,® J. L. Miller, Lorrain, Hans 
and Gillet,® and many others, it appears that we do not deal here with 
a single distinct pathological process, but that many varieties of infec- 
tions of the lungs, bronchi, and pleura are classified under this term; 
the only thing they have in common is that they very frequently 
simulate pulmonary tuberculosis and are treated as such. 

From the clinical standpoint there are two groups to be distinguished 
—the acute and the chronic types. The writer, at times, has had great 
difficulty in recognizing those running an acute course, while those 
of the chronic type, if seen some time after the onset of the disease, are 
very easily differentiated from pulmonary tuberculosis, usually during 
a single examination. 

The acute cases give a history of a sudden onset with fever, malaise, 
cough, and pain in some part of the chest. Those that follow epidemic 
influenza have expectorated more or less blood. Examination at that 

1 Infektion der Lungen durch Streptokokken und Influenzabazillen, Bonn, 1895. 

2 Am. Jour. Med. Sci., 1913, 146, 313. 

3 Tr. Nat. Assn. for Study and Prev. Tuberc., 1915, 11, 140. 

4 Thid., 1916, 12, 170. 


5 Am. Review of Tuberc., 1917, 1, 1. 
6 Rev. de méd., 1919, 36, 173. 


540 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


time shows no changes in the motion nor the resonance of the chest, 
but on auscultation feeble, rarely bronchovesicular, breath sounds and 
moist rales are audible over the greater part of one lobe, usually the 
lower lobe of the left lung. The apex is only rarely affected, and when 
this is the case the diagnosis is extremely difficult. Those who believe 
that in many tuberculous cases the lower lobes are affected at the onset 
of the disease will at once diagnosticate phthisis when finding signs 
of a localized lesion in one of the lower lobes. But although there is 
more or less profuse expectoration of mucopurulent material, no 
tubercle bacilli can be discovered. On the other hand, all kinds of 
streptococci and diplococci may be easily demonstrated in every case. 
The fever abates withina mnth or two, but the physical signs, as well 
as the cough and expectoration, persist for three or four months, and 
finally even these disappear, leaving the patient in excellent physical 
condition. 

The differentiation of these cases from phthisis is made first by 
taking cognizance of the location of the lesion: Basal lesions in tuber- 
culous patients are extremely rare; when they do occur they are ter- 
minal phenomena, when the diagnosis is beyond question. A lesion 
at the base, while the apex is free, should be considered non-tuberculous 
unless the sputum is positive as regards tubercle bacilli. Adhering to 
this diagnostic principle we may avoid nearly all chances of a mistake 
of this kind. In the rare cases showing involvement of the upper lobe, 
it will be noted that the auscultatory phenomena are pronounced, weak, 
or bronchovesicular breath sounds and showers of rales, localized and 
persistent in one apex, but percussion yields a resonant, often a slightly 
tympanitic note. In phthisis such discordance between the findings 
on auscultation and percussion is extremely rare. When such a large 
area of the upper lobe is implicated by a tuberculous process there is 
almost invariably dulness to be elicited above and below the clavicle. 
Similarly the roentgen-ray findings are, as a rule, negative in non- 
tuberculous infections of the lung. 

The chronic cases usually give a history of an acute or subacute 
onset. Many of them are, in fact, recurrences of the original acute 
process. The patient coughs, expectorates more or Jess sputum, has 
pain in the chest, and physical examination shows a distinctly localized 
lesion in one of the lower lobes of the lung, more commonly the left. 
However, in addition to the fact that the lesion is at the base, thus 
showing that it is unlikely to be tuberculous, there are other clinical 
features which tend to show that we are not dealing with tuberculosis. 
Tuberculosis with such extensive involvement is invariably accom- 
panied by symptoms of toxemia, fever, nightsweats, emaciation, ete., 
while in the non-tuberculous cases all this is lacking. The tempera- 
ture is normal, or only slightly elevated some days, and the nutrition 
of the patient is good. He may be gaining in weight despite the per- 
sistence of signs of an extensive lung lesion. The pulse is normal 
and stable, a point which should always be looked for in these cases. 


CHRONIC BRONCHITIS AND BRONCHIECTASIS 541 


The low blood-pressure characteristic of phthisis is lacking. Some 
of these patients, despite the evidence ot moisture within the lung, 
expectorate very little, while others expectorate considerably. Per- 
cussion has been of assistance in some cases. When there is no 
thickened pleura, and this is the case in the majority, the note elicited 
is resonant, and the a-ray findings may also prove negative, while in 
phthisis with such extensive involvement the reverse is invariably 
true. 

Repeated examinations of the sputum give negative results as 
regards tubercle bacilli, but pneumococci, or any of the various strains 
ot streptococci, are to be found in nearly every case. 

These cases are seen in patients of all age periods. They are very 
frequent in children of school age, and because of the erroneous state- 
ment in many books that the lesion in tuberculous children is most 
commonly found in the lower lobe, and that negative sputum is the 
rule, many physicians do not hesitate to diagnosticate tuberculosis in 
these little patients. But it is worth repeating that chronic tuberculosis 
of the lungs in children of school age, when it does occur, affects the upper 
lobe almost invariably, and lesions in the lower lobes should not be con- 
sidered tuberculous unless there are symptoms of toxemia and positive 
sputum. 

The course of these non-tuberculous lung infections is variable. 
Some recover within a few months and no trace of the trouble can be 
found. In others, the acute or subacute symptoms recur at irregular 
intervals, especially after acute “colds” or “grippe” during the winter 
and autumn months. A large number find their way into sanatoriums, 
where they remain for months. I have many patients of this class 
who have taken several ‘“‘cures”’ in institutions, and they still show 
signs of an old lung lesion at one base; they still cough and expectorate, 
though their general health has been, and is, excellent. Although they 
have been told that they are sputum-negative cases, a fact which they 
hardly ever fail to mention, many will not be convinced that their 
trouble is not of a tuberculous nature. 

Chronic Bronchitis and Bronchiectasis.— The average case of chronic 
bronchitis is easily differentiated from pulmonary tuberculosis when 
the following points are borne in mind: Barring those in whom the 
disease is secondary to cardiac or renal disease, and the diagnosis of 
the primary pathological process is clear, those suffering from bron- 
chitis have been subject to colds, have coughed and expectorated for 
many years, perhaps since childhood, and their general health has 
suffered but little, or not at all, as a result of these symptoms. On the 
other hand, phthisical subjects give a definite history of an onset, be 
it ever so insidious, when they began to cough, have fever, languor, 
nightsweats, anorexia, emaciation, etc., symptoms which lack in 
chronic bronchitis. We should not be rash in making a diagnosis of 
tuberculosis in a person who has coughed for many years and his general 
health has not suffered much, unless the signs and symptoms are clear-cut, 


542 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


or the sputum is positive. In chronic bronchitis the harsh bronchial or 
bronchovesicular breath sounds, if present, are tound diffused all over 
the chest, while in tuberculosis they are localized in only one or in both 
apices. Similarly adventitious sounds, especially moist rales, in 
phthisis are found in the upper lobes, while in bronchitis they, are 
audible over the bases, on both sides of the chest. Despite the fact 
that the physical signs denote extensive involvement, the general 
condition of the patient leaves little to be desired, which is never 
observed in phthisis implicating the lower lobes of the lungs. ‘Tuber- 
culous with basal lesions are hectic, marasmic, and soon moribund; 
they usually have laryngeal and intestinal complications. In tuber- 
culosis with such profuse expectoration tubercle bacilli and elastic 
tissue are almost invariably found in the sputum, while in bronchitis 
repeated examinations prove negative. 

Many patients who have been attacked by epidemic influenza with 
complicating pneumonia remain with chronic or subacute bronchitis 
for months, and because of the tradition that influenza is an activator 
of tuberculosis, they are treated as phthisical. Since the recent 
epidemics many such cases have come under the writer’s care. It is, 
however, to be noted that impairment of resonance, the numerous 
large, moist, consonating rales are audible, as a rule, over the bases; 
that the pulse is normal, or rather slow; that the general health is good; 
in fact, the patients may be gaining in weight despite the extensive 
pulmonary lesion. The sputum is negative as regards tubercle bacilli, 
which hardly ever occurs in tuberculous subjects expectorating such 
large quantities. When these points are borne in mind errors can be 
avoided in nearly all cases. 

Bronchiectasis.— Bronchiectasis is not so easily differentiated, and 
many patients with this disease pass through life considered tuber- 
culous. Here we have a localized lesion in the chest exquisitely 
simulating chronic tuberculosis. In fact, many find their way into 
sanatoriums or hospitals for advanced consumptives, where they are 
kept for months and years. I have known numerous bronchiectatics 
who have been admitted to several sanatoriums as far advanced cases 
with negative sputum. In New York City many are kept under 
supervision by the authorities, and followed up to their places of 
employment with a view of preventing the spread of tuberculosis. 
Among 29,700 patients admitted to the Brompton Hospital, London, 
during the last twenty years a clinical diagnosis of bronchiectasis was 
made in 567, or 1.9 per cent, according to Jex-Blake'. This author is 
of the opinion, however, that bronchiectasis was present in fully 5 per 
cent of the patients admitted. 

Bronchiectatie patients give a history of long duration; they have 
coughed and expectorated for many years, perhaps since an attack 
of pneumonia or pleurisy; others, since a surgical operation, during 


1 British Med. Jour., 1920, 1, 591. 


CHRONIC BRONCHITIS AND BRONCHIECTASIS 543 


which general anesthesia was administered, and they began to cough 
soon after regaining consciousness. They state that nile they almost 
always expectorate, the cough tortures them only periodically, with 
frequent remissions of shorter or longer duration, during which they 
do not cough much, but still expectorate “mouthfuls” without any 
effort. Posture, as a rule, has an influence on their cough and expec- 
toration; some cough and expectorate more when lying on the right 
side, while others do so when reclining on the left side. In some the 
sputum is fetid, while in most it differs but little from that brought 
out by advanced tuberculous patients. While the majority of bron- 
chiectatics are afebrile, in many careful thermometry reveals low fever, 
99.5° F. to 101° F. in the afternoon. But the subnormal temperature 
in the morning characteristic of phthisis is usually absent in these 
eases. ‘The pulse 3 is normal, excepting during the advanced stages, 
when there is cardiac dilatation with tachycardia, dyspnea, cyanosis, 
etc. The blood-pressure is normal or high, and only rarely low, as is 
the case in phthisis. A large proportion of these patients spit blood; 
I have seen many in whom the pulmonary hemorrhage was copious, 
and even fatal. A blood count will show an increased leukocytosis 
with a high proportion of polynuclears in bronchectasis, which is rare 
in phthisis. 

It is thus seen that bronchiectasis may easily be mistaken for tuber- 
culosis. The differentiation is made along the following lines: In 
phthisis tubercle bacilli and elastic tissue are almost invariably found 
when the sputum is so profuse. Patients with such large, active 
tuberculous cavities are febrile, cachectic, etc., and often laryngeal and 
intestinal complications are seen; these are all lacking in bronchiec- 
tasis. The tuberculous patient with excavations gives a history of an 
onset, insidious or acute, with fever, nightsweats, etc., while the 
bronchiectatic has recently passed through an attack of pleurisy, 
pneumonia, influenza, etc., or coughed for many years, during which he 
has not shown any decided symptoms of tuberculous toxemia, and has 
retained a good general condition of health; he may even be quite adi- 
pose despite cough and expectoration. ‘The physical examination, in 
the vast majority of cases, decides the diagnosis when we bear in mind 
the following points: 

In phthisis the lesion is nearly always localized in the apex or the 
upper lobe, in bronchiectasis in the lower or middle lobe, most com- 
monly in the left side of the chest, and exceptionally in the upper lobe. 
In phthisis signs of pulmonary retraction are almost invariably found 
—deep excavation of the supra- and infraclavicular fossee; in bron- 
chiectasis these are often fuller than normal. The atrophy of the 
respiratory muscles characteristic of chronic phthisis is lacking in 
bronchiectasis. Dulness, when at all discovered by percussion, is 
found over the upper lobe in phthisis and over the lower lobe posteriorly 
in bronchiectasis. In the latter, more often than in phthisis, the reso- 
nance will be influenced by the presence or absence ot secretions in the 


544 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 





savities—one day when they are full of secretions the note will be dull, 
while another, after the patient has expectorated profusely, it may be 
resonant, despite the fact that there are numerous large moist rales. 
In the uncommon cases of bronchiectasis of the upper lobe there is elicited 
resonance above the clavicle and dulness below it; the reverse 1s almost 
invariable in phthisis. With large tuberculous cavities in one lung 
there are almost always signs of implication of the other side of the 
chest, while bronchiectasis is commonly unilateral. If the case has 
been kept under observation for a long time it will be noted that in 
tuberculosis signs of consolidation precede those of excavation, while in 
bronchiectasis the reverse generally occurs. Bronchiectatic cavities 
remain of about the same size tor many years, often indefinitely, while 
active tuberculous cavities, with large, moist rales, show a decided 
tendency to enlarge. When bronchiectatic cavities involve both sides 
of the chest, which is very rare, they are found irregularly scattered, 
with almost normal lung tissue intervening, while phthisical cavities 
are contiguous extensions of the original apical lesion. It is, in fact, 
very rare to find in phthisical chests signs of more than one cavity with 
more or less healthy lung tissue between the two excavations. In 
multiple bronchiectasis this is the rule. The heart is found displaced 
in both phthisis and bronchiectasis toward the affected side, but there 
is one significant difference which has been pointed out by William 
Ewart: ‘‘The displacement of the heart toward the diseased side in 
the chest in the usual cases of unilateral phthisis follows -an oblique 
direction upward; a horizontal displacement is exceptional and suggests 
some complicating pleural factor. In unilateral bronchiectasis the 
displacement is, practically speaking, always horizontal; not only by 
reason of the basic origin of the disease, but largely also owing to the 
lowering of the diaphragm on the sound side, with extension of the 
cardiac beat into the epigastric notch.” This holds true in the vast 
majority of cases, and is most easily determined with the aid of the 
roentgen-rays. 

Another important distinction is to be mentioned: In bronchiectasis 
the breath sounds are usually feeble, though in some instances they may 
be bronchial; a large number of coarse, moist, consonating rales are 
audible, and the x-rays show only slight opacities, variable, according 
to the fulness or emptiness of the cavities at the time the examination 
is made. In phthisical cavities the 2-rays findings are more accentu- 
ated and more extensive than physical signs would lead us to suppose. 
Scoliosis is a common sign of bronchiectasis—the convexity is turned 
toward the affected side; this is rare in cases with phthisical cavities. 

Pleural Vomicz.— Among the non-tuberculous pulmonary conditions 
treated as advanced consumption, and often sent in to my wards at 
the Montefiore Hospital, are pleural vomicee—localized collections of 
pus in the pleural cavity, originating in the lung, pleura, or even the 
abdominal organs, but burrowing their way to the exterior through a 
bronchus or fistula. These vomice may be found anywhere in the 


PLEURAL VOMICA 545 


chest, but they are most commonly located in the region.of the inter- 
lobar fissure, and at the diaphragmatic pleura. 

The differential diagnosis between pleural vomicee and advanced 
phthisis is very simple in the vast majority of cases. Of first impor- 
tance is a good history of the case. Pleural vomice begin acutely 
with symptoms of pleurisy with effusion. After a variable time the 
acute symptoms abate, and the patient recovers to a certain degree, 
but he keeps on expectorating large quantities, “mouthfuls,” of puru- 
lent matter. In others, there is a history of pneumonia, followed by 
empyema which broke through a bronchus. In still others, there is a 
history of an acute septic process, especially after a surgical operation, 
or after childbirth. Cases have been observed in which the pus in the 
pleural pocket came from an appendicular or hepatic abscess, the pus 
burrowing its way into the pleura, and then through the lung into a 
bronchus to the exterior. 

All cases give a history of an acute disease with fever, perhaps of the 
septic type, prostration, pain in the chest, and either primary or 
secondary pneumonia or pleurisy was diagnosticated at the time. 
The fever lasted a variable time, in some cases several weeks, when it 
suddenly dropped with the appearance of profuse expectoration of 
purulent material. The expectoration may come on suddenly with a 
gush, almost asphyxiating the patient. During the first few days the 
amount brought out is considerable. In a case under my care it was 
more than a pint. Within afew days the amount of sputum decreases, 
but it still remains relatively profuse for an indefinite time. It is 
during this chronic stage that tuberculosis is often diagnosticated. 
These patients cough, expectorate purulent sputum, often have 
hemoptysis, are emaciated, and run a subfebrile temperature, influ- 
enced by the amount of expectoration. When the latter is profuse, 
the fever is negligible, but during days when the communicating bron- 
chus is plugged, the fever is high. The cough and expectoration are 
influenced by posture; some cough more when lying on the affected 
side, while with others the reverse is true, apparently depending on the 
direction of the communicating fistula or bronchus. 

Physical exploration of the chest shows signs of an extensive basal 
lesion, usually simulating the signs of a pleuraleffusion. Infact the first 
thing one thinks of after going over such a chest is fluid, probably pus. 
But exploratory puncture fails to confirm it. In the cases in which 
the vomica is located in the region of the interlobar fissure, the signs 
are those of consolidation, or excavation of the upper part of the 
lung, though careful examination shows that the real apex of the lung 
remains unaffected, a fact which is of great diagnostic significance. 
The affected area is dull, more commonly flat, on percussion, and 
either feeble, cavernous, or amphoric breath sounds are heard, depend- 
ing on whether the cavity is filled with secretions or empty at the 
time of the examination. Large, moist rales, of a consonating charac- 
ter, are audible over the affected area. 

35 


046 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


The differential diagnosis between this condition and phthisis is 
thus clear: The history points to an acute onset, as pleurisy or pneu- 
monia, or following some other septic process; the lesion is localized in 
the lower lobe, or in the region of the interlobar septum, while the apex 
of the lung remains free. These, combined with the fact that, despite 
its abundance, the sputum is negative, rules out tuberculosis. We have 
repeatedly emphasized that when the apex shows no signs of a leston 
only positive sputum should justify the diagnosis of phthisis. 

Abscess of the Lung.— At times patients with pulmonary abscess, 
especially the chronic form, are treated as advanced consumptives. A 
consideration ot the history of the case should clear up the diagnosis in 
most cases. Itis often preceded by an attack of aspiration pneumonia, 
mainly after an operation, very often after tonsillectomy, or after a 
septic pulmonary embolism. ‘There are hectic fever, sweating, emacia- 
tion, and spasmodic cough, expelling large quantities of sputum which 
differs, as a rule, from that observed in phthisis. It has a brown color, 
due to an abundance of hematoidin crystals and elastic tissue fibers 
which may be found microscopically. In rare instances it is fetid, 
but not as offensive as that of gangrene of the lung. Hemoptysis, at 
times copious hemorrhages, occur, and it is often this symptom that 
suggests phthisis to the patient and the physician. But here again the 
location of the lesion should clear up the diagnosis. It is usually in 
the lower lobe, while the apex remains free from pronounced patho- 
logical changes. I have seen several cases in which the lesion was in 
the upper lobe, especially in diabetics, or in persons on whom operations 
on the lower jaw were performed. Many of my cases began soon after 
operations on the tonsils. But all in all, the history, the fact that the 
apex is free, the character of the sputum, and the absence of tubercle 
bacilli, are diagnostic points. 

Gangrene of the Lung.—When occurring as a sequel to aspiration 
pneumonia, pulmonary embolism, or after operations on the jaw in 
diabetics, or to the entry into the bronchi of foreign bodies such as 
teeth, fishbones, etc., gangrene of the lung is easily distinguished from 
phthisis by the history alone. But when occurring as a complication of 
bronchiectasis it is, at times, mistaken for tuberculosis: The history 
of cough and expectoration for many years is apt to prove misleading. 
When severe pulmonary hemorrhage is one of the symptoms, the diag- 
nosis of tuberculosis is fortified. 

But fetid sputum is exceedingly rare in phthisis; as rare as gangrene is 
as a complicationof phthisis (see p. 563). Gangrene is characterized by 
high irregular fever, prostration, cough, and expectoration of consider- 
able quantities of fluid, frothy, and highly offensive sputum which 
separates into three layers, the lowermost containing fragments of 
lung tissue. Elastic tissue is only rarely found in the sputum because 
it is soon destroyed by the rapid action of the pathogenic agent, but 
at times fragments of lung tissue may be discovered. None ot these 
clinical features are seen in pulmonary tuberculosis, excepting when 
gangrene appears as a complication. 


ab f S, 


Fie 1 


AXLV 


HirGen2, 





Pleural vomica. Dense homogeneous 
shadow in lower third of left side of the 
chest. Several dilated bronchi in left 
hhilus region. Obliteration of left costo- 
phrenic sinus and displacement of the 
heart to the left. Note the absence of 
changes in the apices. 


isitey 3 





Multiple bronchiectasis. Diffuse shadow 
in right hilus, middle lobe and portions 
of axillary regions, studded with bronchiec- 
tatic cavities. Obliteration of costophrenic 
sinus; pleuropericardial adhesions. Marked 
peribronchial changes in left lung. Supra- 
clavicular fields practically free from 
changes. 


Fic. 4 





Bronchiectasis. 


cavity with 
thick walls in upper lobe of right lung; 
thick pleura with dilated bronchi in lower 
lobe; elevation of diaphragm. Left lung 
emphysematous; calcified nodule in second 
interspace. Dextrocardia. 


Large 


Metastatic hypernephroma of the lung. 
Autopsy. Sent in as tuberculous. Opaci- 
ties denoting infiltration of both apices. 
Effusion (hemorrhagic) into right pleura. 


PLATE XXV 


lives, 1! Fic. 2 














Fie. 3 ; Fic. 4 





| Malignant tumor of the left lung. In the first roentgenogram the shadow could 
hardly be differentiated from a tuberculous lesion. It was only in the third roentgeno- 
gram, taken three months later, that the true nature of the affection could be made out 
roentgenographically. 


CANCER OF THE LUNG 547 


Cancer of the Lung.—Intrathoracic neoplasms, especially carcinoma 
.and sarcoma of the bronchi, lung, pleura, and glands, are often mistaken 
for tuberculous disease of the lung. The onset is insidious with cough 
and mild fever, the curve in some cases under my care having exqui- 
sitely simulated that seen in typical cases of incipient tuberculosis. 
When to this are added hemoptysis of various degrees, and loss in 
weight, it is clear that there are strong reasons for thinking of tuber- 
culosis, the more common disease. Moreover, malignant disease of 
the lung is likely to pursue a very slow course. 

The differentiation is made by the symptomatology, and the physical 
signs as well as with the aid of the x-rays, though I consider the a-ray 
findings less reliable in early cases than rational interpretation of signs 
elicited by exploration of the chest (see Plates XXIV and XXYV). 
While growing, the tumor gives rise to certain pressure symptoms which 
are of immense value in the differential diagnosis. Pressing upon the 
superior vena cava, enlarged veins on the chest wall and shoulder or 
anterior part of the neck are produced; pressure on the sympathetic 
will dilate the pupil on the affected side. There may be a difference 
in the fulness of the pulse when the two radials are compared. These 
signs are invaluable, but they are more often absent as present. 

At the beginning of the disease, when the new growth is yet insig- 
nificantly small, the physical signs may not show any alterations in the 
resonance and breath sounds, and the constitutional symptoms of 
tuberculosis may be so striking as to mislead. But it appears that in 
nearly all cases, even those showing a subfebrile temperature, the pulse 
is normal, which is rare in tuberculosis. Pain in the chest, and tender- 
ness of the skin of the affected side are characteristic of tumor, but rare 
in phthisis. Dyspnea is very common in tumor, rare in phthisis. In 
some cases I have noted symptoms and signs of pulmonary emphysema, 
with slight fever and hemoptysis. Here again the diagnosis was diffi- 
cult and required prolonged observation before a conclusion could be 
arrived at. 

With the growth of the tumor, local signs may be made out by 
physical examination. If the neoplasm is located in the upper part of 
the chest, the signs again simulate tuberculosis, but a careful analysis 
of the findings usually shows striking differences. Emaciation appears 
early in phthisis, while in cancer of the lung the nutrition of the patient 
may leave little to be desired for many months. Even in the later 
stages, when the patient loses in weight considerably and progressively, 
the cachexia differs markedly from that of tuberculosis. In the latter 
the patient appears hectic, while in the former the waxy yellow tinge 
of cancerous cachexia is almost invariably noted at first sight; the 
severe blanching of the face also betrays malignant disease. But, as 
was already stated, cachexia appears late in intrathoracic tumor, 
while in tuberculosis it is often an early symptom. 

Percussion over the site of the tumor elicits a flat note, which is 
never found in tuberculosis of the upper lobe, Moreover, above the 


> 


548 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


area of flatness there may be an area of resonance, again unknown in 
tuberculous lesions. The affected side of the chest in many cases may: 
thus be found to be made up of three zones: an upper, resonant one, 
above the second rib; a middle one, from the second rib for one or two 
interspaces, which is flat, and the lowermost again resonant. The upper 
area of resonance should immediately excite suspicion. When the 
growth appears first in the lower parts of the chest tuberculosis should 
not at all he thought of, but often pleural effusion is simulated, but 
this is excluded very easily, in most cases by the history, course, and 
physical signs. 

Auscultation also gives very valuable clues. If the tumor is of some 
dimensions, there will be noted feeble or complete absence of breath 
sounds over the circumscribed area which has been found flat on per- 
cussion. Now, in tuberculous lesions with such extensive implication 
there are almost invariably to be heard adventitious sounds, usually 
large, moist, and consonating rales. It may be stated that a very dull or 
flat note, with feeble breath sounds, without any rales is strongly suggestive 
of a tumor. ‘The reasons for the absence of breath sounds are these: 
The tumor often arises from the wall of a large bronchus and with 
its growth it compresses the air tube; or when one of the mediastinal 
glands is the source of the tumor, its growth may compress a large 
bronchus in its vicinity. The result is atelectasis of the lobe supplied 
by this bronchus—flatness, absent breath sounds, etc., but no rales. 
Again, such extensive tuberculous involvement is accompanied by 
adventitious sounds. These signs, combined with the lack of the toxic 
symptoms of phthisis, especially the lack of tachycardia, are sufficient 
to direct attention to the problem of malignancy, even in the presence 
of such symptoms as cough, slight fever, hemoptysis, ete. 

With the growth of the tumor the area of flatness increases, the veins 
on the chest become more and more prominent, and at times metastatic 
deposits are discovered in the glands above the clavicles, ete. A good 
sign to be considered is the position of the trachea and the heart: 
In tuberculosis with such extensive involvement these two organs are 
drawn toward the affected side, while in cancer of the lung they are 
pushed away toward the unaffected side. This sign has served me 
often in doubtful cases. In the later stages of cancer, when the tumor 
become gangrenous, and fetid sputum is expectorated, the mediastinum 
may be drawn toward the affected side, as has been noted by the writer 
in rare instances. 

Malignant tumors of the pleura or lung are complicated by pleural 
effusions in over 50 per cent of cases. In many the fluid is serous, in 
others, serosanguineous, while at times it is purulent. If the diagnosis 
has not been previously made the difficulties increase when this occurs. 
The fluid is often sanguineous, but this does not help us, because it is 
often so in phthisis. ‘The pressure signs enumerated above are, how- 
ever, more likely to occur in cancer. A careful watch for metastases 
may clear up an otherwise obscure case. We must, however, again 


ACTINOMYCOSIS 549 


emphasize that when blood is found at the first exploratory puncture, 
it is of greater diagnostic significance than when found at the second 
puncture, because tapping the chest, at times, causes bleeding, thus 
coloring the effusion. Purulent effusions are not uncommon in cancer. 
At times fragments of the growth or characteristic cells are found in the 
centrifuged specimen of the aspirated fluid, but this is rare in my 
experience. It has been stated that when a large number of coarsely 
granular eosinophile cells are found in the fluid it is a good sign of tumor 
of the pleura or lung. 

One characteristic of effusions in cases of cancer of the lung is that 
they fill the entire pleural cavity; at least, flatness is elicited while 
percussing the chest from above the clavicle down to the diaphragm, 
and this is a sign which has hardly ever failed the writer in cases in 
which fluid in the chest was the first thing seen when the patient is 
examined. In inflammatory pleural effusions the resonance above the 
upper level of the fluid is more or less tympanitic—skodaic. In 
hydro- and pyopneumothorax, it is shifting. In cancer of the pleura 
or lung it apparently fills the entire chest, which is exceedingly rare, 
if it ever occurs, in effusions due to other causes in which there is at 
least resonance above the clavicle. 

The writer! has recently aspirated fluid in the chest and replaced it 
with air in the usual way in which a pneumothorax for therapeutic 
purposes is induced. A tumor is then made much clearer on the 
roentgenographic plate than can be expected otherwise. Similarly a 
diagnostic pneumothorax is induced in cases without fluid with a view 
of bringing out the outlines of an intrathoracic neoplasm. 

I have observed several in cases in which the first symptoms and 
signs were those of pulmonary emphysema, only the persistent unpro- 
ductive cough, slight fever, and hemoptysis drawing the attention of 
the patient to the seriousness of the disease. The dyspnea may be 
severe, and in one case it was even distinctly stridorous, due to pressure 
of the growth or the implicated tracheal glands on the trachea. Ina 
few cases I have seen distinct pulsations of the thorax, especially when 
the tumor appeared in the upper part of the chest. These pulsations 
could be perceived by palpation. These signs are not all present in 
every patient, still some may be found in each case, and should be 
considered before a diagnosis is made. 

Actinomycosis.—Actinomycosis of the lung, in its initial stages, 
presents symptoms and signs not unlike those of pulmonary tubercu- 
losis. There are cough, loss of flesh, mild fever, ete. So long as the 
fungus remains within the lung there may be little or no expectoration 
and the sputum is microscopically negative. When it makes its way 
into a bronchus, a microscopic examination may reveal the fungus, 
if it is looked for. When it reaches the pleura, symptoms of pleurisy 
with effusion arise and the patient is for a time treated for tuberculous 





1 Jour. Am. Med. Assn., 1921, 76, 581. 


550 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


pleurisy or empyema. The constitutional symptoms in advanced 
cases of actinomycosis simulate those of active and advanced phthisis 
very strikingly. There are hectic fever, tachycardia, emaciation, 
cough, and expectoration of large quantities of nummular sputum, 
hemoptysis, ete. 

In the initial and latent stages actinomycosis differs from phthisis 
in the following points: ‘Tuberculosis lesions begin at the apex almost 
invariably, while actinomycosis is usually localized in the middle or 
lower lobe. We have already repeatedly warned against a diagnosis of 
tuberculosis when the apex remains unaffected. There are, however, 
cases of actinomycosis in which the upper lobe of the lung is the first 
to be affected. Because at this stage tubercle bacilli and elastic tissue 
may be absent in phthisical patients, the difficulties are at times 
unsurmountable. A careful search should be made for the ray fungus 
in all doubtful cases. 

The diagnosis is usually cleared up within a few weeks when a fluc- 
tuating swelling appears on the chest wall, which may suggest empyema 
necessitatis, especially since there are also signs of a pleural effusion. 
But an examination of the sputum, or of the pus removed from the 
external swelling, shows yellowish granules or streaks of actinomycotic 
growth. 

Streptotrichosis of the Lung.—Nocardia.—Infection with any of 
the microérganisms of the streptothrix group may give symptoms which 
are often mistaken for those of chronic pulmonary tuberculosis. Of 
late, many cases have been reported in this country, while in Europe 
these infections have been described as pseudotuberculosis. In 1898 
Simon Flexner! described a case of this “pseudotuberculosis” with 
autopsy. More recently Edith J. Claypole,? William M. Stockwell,? 
and others, have reported cases in this country. 

The symptoms are those of chronic phthisis. ‘The onset is slow and 
insidious. The patient coughs, expectorates mucopurulent material, 
and is short-winded. Hemoptysis is not uncommon though profuse 
pulmonary hemorrhages are not observed. Either streaky sputum or 
small amounts of blood are brought out. ‘The symptoms of toxemia, 
such as fever, nightsweats, tachycardia, etc., are usually wanting. 
Most patients present a rather good external appearance despite the 
symptoms of pulmonary trouble which may have lasted for years. It 
seems that most patients are treated as tuberculous with negative 
sputum, and are admitted to sanatoriums and hospitals for advanced 
consumptives. 

The differential diagnosis can only be made by a microscopical 
examination of the sputum, of which large quantities should be obtained 
for the purpose. Inasmuch as the staining methods employed to 
discover tubercle bacilli render the streptothrix invisible, and some of 


1 Jour. Exper. Med., 1898, 3, 435. 
2 Arch. Int. Med., 1914, 14, 104. 
3 Tr. Nat. Assn. for Study and Prev. Tubere., 1916, 12, 265. 


BRONCHOPULMONARY SPIROCHETOSIS 551 


the stains are acid-alcohol-tast, great care should be taken in gauging 
the amount of the decolorization of the carbol-fuchsin preparations, 
which should be varied so as to differentiate the less acid-fast types. 
The Gram-method of staining may also be employed. ‘There are strong 
reasons for believing that it special care were taken with all sputum- 
negative cases showing signs of chronic tuberculosis, more cases of 
pulmonary streptotrichosis would be discovered. Claypole! believes 
that she has worked out a certain serological reaction which she recom- 
mended as of diagnostic value in streptothrix, but considering the large 
number of types of this microérganism, it is problematical whether a 
single skin reaction will be efficient diagnostically. 

Bronchopulmonary Spirochetosis.—Hemorrhagic Bronchitis. — This 
disease was first observed in Ceylon and described by A. Castellani in 
1905. Later Jackson reported cases in the Philippine Islands, and 
during the World War, many cases were discovered among the 
troops in France, Belgium, Italy, England, Switzerland, ete. In a 
soldiers’ sanatorium in Northern Italy, Castellani? found that 3 per 
cent of the patients sent in with the diagnosis of pulmonary tuber- 
culosis, in reality suffered from bronchopulmonary  spirochetosis. 
Similar experiences have been recorded in France. 

The symptoms are akin to those of pulmonary tuberculosis, and most 
patients are treated as such. As given by H. Violle,’ there is cough, 
more or less copious expectoration, but fever is lacking in the majority 
of cases, while the general condition of the patient leaves little to be 
desired. Violle states that the gross appearance of the sputum is 
characteristic and that a diagnosis can be made by examining it alone. 
The expectoration is viscid, uniformly thick and closely resembles the 
juice of gooseberries. But what makes the symptomatology like that 
of phthisis is the pulmonary hemorrhage which is never lacking. ‘The 
blood brought out may be considerable and is of a peculiar pinkish 
color; fatal hemorrhage, however, never occurs. P. Nolf and P. Spehl! 
describe cases without hemoptysis. If these cases the sputum was 
mucopurulent, yellowish-green in color, and after some days became 
fetid, the fetor remaining pari passu with the number of spirilla. 

Physical exploration of the chest may reveal nothing, or some signs 
of bronchitis may be discovered. In rare cases signs of consolidation 
of an apex or any part of the lung have been found. 5S. Fishera’ 
reports cases of apical catarrh running a chronic course with fever, 
loss of flesh, nightsweats, and blood-stained sputum containing spiro- 
chet, but no tubercle bacilli. 

Several cases were admitted to the Montefiore Hospital as tuber- 
culous.6 The symptoms and signs were those of a pulmonary abscess 
Jour. Exper. Med., 1913, 17, 99. 

Presse Méd., 1917, 25, 377. 
Bull. Acad. de Méd., Paris, 1918, 79, 429; Lancet, 1918, 2, 775. 
Arch. Méd. Belges, 1918, 71, 1. 


Riforma Medica, 1918, 34, 384. 
6 Fishberg and Kline, Arch. Int. Med., 1921, 27, 61. 


op wo De 


052. DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


with pain in the chest, high continuous fever, incessant cough and 
copious expectoration of offensively fetid sputum. Spirochetee and 
fusiform bacilli were found in the sputum, and, at the autopsy, in the 
pulmonary tissues. However, these organisms were also found in the 
gums of patients who suffered from severe pyorrhea, and the impression 
was gained that the lungs, at least in these cases, were infected by the 
spirochete derived from the buccal mucous membrane. In another 
case in which these organisms were found in the sputum there was 
also pyorrhea. This patient suffered from a chronic bronchial disease, 
and the signs were not unlike those of fibroid phthisis. 

The differentiation from phthisis can be made only by a microscopic 
examination of the sputum. The spirochete bronchialis and fusiform 
bacilli are found in large numbers; in some cases the specimens are 
actually teeming with them. They may be stained with the Roman- 
owski stain, but the silver nitrate stain of Fontana-Tribeudeau is 
superior. The organism is extremely variable in shape, length, and 
number of spirals. It has not yet been cultivated, but Chalmers and 
O'Farrell have succeeded in inoculating monkeys by intratracheal 
injections of a patient’s sputum. The prognosis is generally favorable 
in acute cases, though in those developing pulmonary abscess, as the one 
observed by the writer, a fatal issue is the rule, but when the disease 
runs a chronic course it may last indefinitely, with occasional remissions. 

The differentiation from phthisis is thus made by the following 
criteria: Absence of tubercle bacilli, of hyphomycetes, and of ova of 
Paragonimus westermanii from the sputum, while the Spzrochete 
bronchialis and fusiform bacilli are found. 

Pulmonary Lesions in Cardiac Patients.— Patients suffering from 
organic heart disease, especially mitral stenosis, often cough, expecto- 
rate, spit blood, have mild fever, and are emaciated, and for these 
reasons are very frequently treated for tuberculosis. Several cases ot 
mitral stenosis are annually sent into my wards in the Montefiore 
Hospital as tuberculous, and in my private practice I have very fre- 
quently cases presented to me as tuberculous, though they only suffer 
from mitral obstruction. The main reason is the frequency of hemop- 
tysis in mitral stenosis, which is, as has already been mentioned, next 
in frequency to tuberculosis a cause of blood spitting. The amount 
of blood expectorated may be slight, only streaky, and in rare cases 
even copious. I have observed it in fully compensated cardiac lesions, 
and in those with signs of decompensation. In the former, the hyper- 
trophied heart pumps the blood through the pulmonary vessels with 
great vigor, and because of the obstruction it meets while passing 
through the narrowed mitral valve the pressure is increased, rupturing 
some of the capillaries. It is for this reason that we meet at times with 
hemoptysis in patients in whom compensation is as perfect as could 
be expected. In cases of heart failure also hemoptysis occurs, at times, 
due to hemorrhagic infarction or embolism; though embolism may be 
said to be an infrequent cause, and when it does occur, it is due to an 


1 
On 
CO 


PULMONARY LESIONS IN CARDIAC PATIENTS . 


~ 


& 


antemortem clot in the right auricular appendix. The symptoms are 
clear-cut, but I have seen many in which tuberculosis was diagnosti- 
cated. It usually occurs suddenly, producing acute pain in the chest, 
dyspnea, orthopnea, cyanosis, and hemorrhage, at times very copious. 
In other cases the bleeding is due to thrombosis of the pulmonary 
vessels, and then the accompanying symptoms are less acute. 

In rare instances hoarseness in addition to the cough and hemoptysis 
may suggest tuberculosis when the real trouble is mitral stenosis. 
Osler,! Frischauer, Alexander, Hofbauer, and others, have drawn 
attention to hoarseness, and a brassy or stenotic cough as a symptom 
of mitral stenosis. In a case reported by Osler it was found at the 
autopsy that the left recurrent laryngeal nerve was compressed against 
the arch ot the aorta and the ligamentum Botalli by the dilated left 
auricle and has shown degenerative changes. 

In chronic cases of mitral stenosis in which cough, emaciation, hemop- 
tysis, ete., suggest a tuberculous process the following ‘points of differ- 
entiation are to be borne in mind: Dyspnea on exertion is more pro- 
nounced in cardiac than in pulmonary patients. We have already 
shown that dyspnea is not one of the cardinal symptoms of phthisis in its 
early stage (see p. 278). Rest for afew days may relieve the dyspnea 
of cardiacs. The cough in cardiacs is aggravated during the cold 
weather, or when the patient walks against the wind, and not influ- 
enced much by sedative medication (heroin, codein, etc.) which relieve 
the cough in the tuberculous. Digitalis, however, often relieves the 
cough in cardiacs. In the tuberculous the heart is smaller, at least not 
larger, than normal, while hypertrophy or dilatation may be made out 
in nearly all cases of mitral stenosis. 

Physical exploration of the chest may show some areas of atelec- 
tasis, catarrh, or localized pulmonary edema, simulating phthisical 
lesions. Owing to brown induration, the signs elicited over the apical 
area are those of consolidation, in some cases. In most eases, however, 
the resonance above the clavicle is not impaired. Tales, when heard, 
are found over the lower parts of the chest and bilaterally, and they 
are not constant, because they are due to localized edema of the lung. 
The cardiac murmur characteristic of mitral stenosis usually decides 
the diagnosis. In the rare cases of mitral stenosis without murmurs, 
or when the murmur disappears owing to decompensation, we usually 
find an accentuation or reduplication of the second sound in the second 
intercostal space near the left border of the sternum. At the apex 
the first sound often has a snapping character and on palpation a systolic 
tap or shock may be felt. Percussion shows enlargement of the area 
of cardiac dulness, and in cases of decompensation some form of 
arrhythmia, usually that of auricular fibrillation, may be noted, all 
of which are lacking in phthisis. 

These signs should be sought for in every case of cough and hemop- 


1 Arch. gén. des malad. d. coeur, 1909, 53, 35; Jour. Am. Med, Assn., 1908, 4, 205. 


554. DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


tysis in which the signs of pulmonary tuberculosis are not clearly 
noted. While it is possible that patients with mitral stenosis should 
become tuberculous, yet this is exceedingly rare. In fact, zt has been 
my rule never to diagnosticate tuberculosis in one showing signs of disease 
of the mitral valve and cardiac hypertrophy or dilatation, irrespective of 
the physical signs elicited while examining the lungs, unless the sputum 
reveals tubercle bacilli. I have hardly seen more than a dozen cases of 
mitral stenosis developing phthisis. 

Pulmonary infarction occurring during the course of cardiac disease, 
or from an embolus arriving from some distant diseased vein, may 
be a source of error, as I have seen in several cases. The patient 
knows that he has an organic heart lesion, or phlebitis, and perhaps 
has been treated for these conditions. Suddenly, without any warning, 
he is seized with severe pain in the chest, distressing dyspnea, or 
orthopnea, and hemoptysis. In some the bleeding is very copious, 
even threatening life. After the acute symptoms have been amelio- 

rated, an examination shows signs of a localized area of diseased lung: 
Impaired resonance, feeble, or bronchial, breath sounds, and moist 
rales. These physical signs are mostly found i in one of the lower lobes, 
but may also occur in the middle or upper lobes, especially in the inter- 
scapular space. But the history, as well as the signs of a cardiac lesion, 
or of phlebitis, should clear up the diagnosis in most cases. However, I 
have seen many patients with mitral stenosis, or with remnants of 
pulmonary infarction, treated for an indefinite period in tuberculosis 
clinics in New York City, and others who have been admitted to 
sanatoriums and kept there for months. 

In acute endocarditis and pericarditis, rheumatic or infectious, 
symptoms of tuberculosis may be present. There are fever, tachy- 
cardia, emaciation, hemoptysis, and some of the physical signs of acute 
miliary tuberculosis. In most cases no murmur is audible, and the 
area of cardiac dulness may not be found increased perceptibly. 
When to all this there is added a pleural effusion, which is not uncom- 
mon, the diagnosis of tuberculosis appears inevitable. But a careful 
inquiry into the history of the onset of the disease, as well as the fact 
that the pleural effusion is bilateral, should excite suspicion. Patients 
with acute articular rheumatism, when showing some signs or symp- 
toms of tuberculosis, should not be considered tuberculous without 
positive proof, or a careful study of the course of the disease. Signs 
of pericardial effusion are also indications that we are dealing with a 
cardiac, and not with a tuberculous lesion. 

Syphilis of the Lung.—Syphilis of the lung is an extremely rare 
disease, and when it does occur it is very difficult of diagnosis patho- 
logically as well as clinically. According to Osler,! of 2500 autopsies 
at Johns Hopkins Hospital, lesions which were believed to be syphilitic 
were present only in 12 cases. In a study which included all the 


1 D’Arcy Powers’ System of Syphilis, London, 1914, 3, 15. 


Peep hex AV Tt 


Fic. 1 





Syphilis of the lung simulating in the 
roentgenogram a tuberculous lesion in 
the right apex. 


HitGsee 





Moderate calcification at the hilus on 
both sides. Right diaphragm elevated. 
Heart enlarged, aorta dilated. Both 
apices free. Clinical diagnosis, syphilis of 
the lung. Admitted as tuberculous, and 
treated as such for many years. 


Jail, 2 





Pulmonary syphilis. Diffuse peribron- 
chial infiltrations of right lung, mostly 
marked at the lower half. Hilus glands in 
left lung are distinctly enlarged. Peri- 
ae adhesions mainly seen in right 
side. 





Malignant growth; empyema. Homo- 
geneous shadow obscuring left lung field. 
Because of the fluid and the heart is pulled 
toward the left, the roentgenogram cannot 
decide whether it is due to a thick pleura 
and parenchymatous lesion, or solely to 
effusion. Right lung emphysematous and 
also shows a slight infiltration of the apex. 


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THE LIBRARY. 
OF THE | 
UNIVERSITY OF ILLINOIS 





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SYPHILIS OF THE LUNG 


London Museums, J. kX. Fowler! was only able to discover 12 speci- 
mens, and 2 of these were of a doubtful nature. Among 6000 cases 
of syphilis at 6 hospital at Copenhagen, syphilis of the lung was 
observed only in 2; and among 18 patients with acquired syphilis who 
came to autopsy, Panimiatous lesions of the lung were found 3 times. 
Chiari? found only 2 cases of syphilitic lesions of the trachea and 
bronchi, and 1 of syphilis of the lung. Petersen among 88 autopsies of 
patients with acquired syphilis found lung lesions only in 11. 
The rarity of pulmonary syphilis, despite the fact that syphilis is so 
widespread, testifies that errors in diagnosis are at least as rare as the 
disease. But now and then we meet with a case which shows symptoms 
simulating pulmonary tuberculosis and treated as such. 

Syphilis of the lung manifests itself by the usual symptoms of 
chronic pulmonary tuberculosis, such as cough, expectoration, slight 
fever, loss in weight, and at times even hemopty sis. But it appears 
that in nearly all cases the course of the disease is rather slow; in none 
of the cases observed by the writer has the disease pursued a progres- 
sive course, nor has it perceptibly disabled the patient. Physical 
exploration of the chest shows that the lesion is localized in the lower 
or middle lobe, and the apex remains practically free from changes. 
This alone should excite suspicion that it is not tuberculous. A careful 
search should be made for the stigmata of syphilis in the bones, skin, 
larynx, rhinopharynx, eyes, etc. The Wassermann reaction may be 
of help, but not so much as would be anticipated, because it is fre- 
quently positive in tuberculosis, and phthisical subjects may have had 
syphilis. In fact, the two diseases are found concurrently very fre- 
quently. (See p. 598.) Absence of tubercle bacilli from the sputum 
is no criterion, because in really syphilitic phthisis the amount expec- 
torated is rather scanty, at least in the early stages. 

The differentiation is best made by the application of the thera- 
peutic test. Properly administered doses of arsphenamine, mercury, 
or iodide of potassium will promptly remove the symptoms of syphilitic 
phthisis. In some of my cases the effect was very prompt, within a 
couple of weeks the cough disappeared, weight and strength returned, 
and the patient considered himself well. But this does not imply 
that in the least suspicious case a diagnosis of syphilis of the lung 
should be made and treatment applied. Patients with pulmonary 
tuberculosis are often harmed by antisyphilitic treatment, especially 
mercury and the iodides. Considering the extreme rarity of syphilis 
of the lung, it is clear that Fowler’s suggestions should always be 
borne in mind: (1) The cases must be complete, that is, the symptoms 
observed during life must be considered in connection with the lesions 
discovered on postmortem examination. (2) The evidence of syphilitic 
infection must be undoubted. (3) Repeated examinations of the 


1 Diseases of the Lungs, London, 1898. 
2 Quoted from F. Balzer, Brouardel-Gilbert-Thoinot, Traité de Médecine, Paris, 1910, 
29, 641. 


556 DIFFERENTIAL DIAGNOSIS OF PULMONARY TUBERCULOSIS 


sputum must have been made, and tubercle bacilli have been invari- 
ably absent, and the absence of tubercle from the lungs as the cause 
of the lesions must be proved by postmortem examination. (4) 
Syphilitic lesions about the nature of which there can be no doubt 
must be found in other organs. 

Many tuberculous patients also suffer from syphilis, as has already 
been mentioned. When tubercle bacilli are implanted on a syphilitic 
subject the course of phthisis is rather favorably influenced, probably 
because it is characterized by a tendency to the production of con- 
nective tissue (see p. 598). It must always be borne in mind that the 
presence of syphilis does not exclude phthisis, but that the latter is 
very often engrafted on the former. 

Hyperthyroidism.—The syndrome of hyperthyroidism, which is so 
commonly met with in young persons, and in women during the 
menopause, is very frequently mistaken for phthisis. The acceleration 
of the pulse-rate, the frequent sweating at the least provocation, the 
slightly elevated and unstable temperature and the tendency to fatigue 
and languor, emaciation, and in women menstrual disturbances, are 
suggestive of the symptoms of early phthisis, especially when the 
patient coughs for any reason. On the other hand, symptoms and 
signs of disturbance of the autonomic nervous system are very fre- 
quently seen in phthisis, as has recently been shown from studies of 
Meyer Solis-Cohen,! Sabourin,? Sergent,® Boas, and others. Many cases 
of the milder grades of hyperthyroidism are therefore treated for 
tuberculosis. 

The severe cases of this syndrome, those showing the cardinal signs 
of Graves’s disease, goiter, tachycardia, tremor, and exophthalmus are 
not likely to be mistaken for phthisis, unless the latter appears as a 
complication of the former. But mistakes may be avoided even in 
the milder forms of hyperthyroidism when the following points are 
considered: Patients with tachycardia, liability to sweat at the least 
exertion or excitement, languor, dermographism, etc., are not to be 
considered tuberculous unless a physical examination of the chest, and 
perhapsroentgenography, reveals a distinct pulmonary lesion. Indoubt- 
ful cases it may be advisable to wait for the results ot repeated sputum 
examinations. Otherwise the characteristic symptom of hyper- 
thyroidism, rapid heart action, palpitation, fatigue, flushes, sweats 
more during the day than during the night, a slight tremor of the 
fingers, etc., are sufficient to define the nature of the trouble. In 
some cases, showing signs of collapse induration (see p. 537), only 
prolonged observation will clear up the diagnosis. 

In this connection it is important to mention, a point which is 
strongly emphasized elsewhere in this book (see p. 607), that symptoms 
of hyperthyroidism are very frequent in patients with incipient phthisis, 

Am. Rev. Tubercul., 1917, 1, 289. 


1 
2 Arch. d. Méd., 1919. 
3 Paris Méd., 1920, 10, 80. 


HYPERTHYROIDISM 557 


but that this indicates a good prognosis. In fact, it may be stated that 
hyperactivity of the thyroid is incompatible with progressive phthisis 
within certain limits. There is therefore no reason to make a hasty 
diagnosis in patients who cough, present some indefinite signs of an 
apical lesion, and incidentally show symptoms of hyperthyroidism. 
If the lesion is tuberculous, even when tubercle bacilli are found in the 
sputum, which is very rare, the outlook for recovery is excellent in the 
vast majority of cases, and the chances are that we are not likely to 
lose much by delaying treatment for tuberculosis. 

There are good reasons for believing that the syndrome recently 
described as neurocirculatory asthenia, and which some believe to be 
one of the manifestations of hyperthyroidism, is also not likely to 
develop into phthisis. 


CHAPTER XXIX. 


COMPLICATIONS OF PHTHISIS. 


Mosr of the pathological processes described as complications of 
phthisis are part and parcel of the tuberculosis process, or symptoms 
of the disease which, at times, assume the ascendency. This is the 
case with hemoptysis, ulceration and amyloid degeneration of the 
intestines, tuberculosis of the larynx, kidneys, meninges, ete. Many 
of these conditions have been discussed while speaking of the sympto- 
matology of phthisis. Pleural complications, such as pleurisy, pneu- 
mothorax, ete., are treated in special chapters. Here a few of the 
more important complicating processes, which may have an influence 
on the course or the prognosis of pulmonary tuberculosis, will be 
discussed. 

Laryngeal Tuberculosis.—The frequency of this complication 
during the course of phthisis has been differently stated by various 
authors. The proportion varies from 5 to 50 per cent. Harold Bar- 
well found at the Mount Vernon Sanatorium 11.69 per cent among 
1541 tuberculous patients; Brandenburg, 9.16 per cent; John B. 
Hawes,' only 8 per cent among 1245 patients. Even sanatoriums, 
which do not admit patients with laryngeal complications, have 
many with this disorder. Thus at Otisville, N. Y., Julius Dworetzky? 
found that 25.6 per cent had laryngeal tuberculosis. Among 100 
tuberculous children under fourteen years of age Dworetzky found no 
case of laryngeal tuberculosis. It seems that the proportion found 
depends on the zeal displayed by the laryngologists looking for it. 
Percy Kidd’ found that 50 per cent of fatal cases of phthisis showed 
tuberculous laryngitis at the autopsy, and of these only 20 to 50 per 
cent were recognized during life. The estimate that one out of three 
patients with active and progressive phthisis has a laryngeal lesion 
appears to be correct. 

Laryngeal tuberculosis spells phthisis; primary tuberculosis of this 
organ is so exceedingly rare as to constitute a medical curiosity. It is 
more frequent among males than among females, the proportion being, 
according to Morel Mackenzie, 2.7 of the former to 1 of the latter. 
The reason for this disparity 1s that men are altogether more liable to 
throat affections, probably because of the abuse of tobacco, alcohol, 
and exposure to irritation by dust at their occupations. It is also 
likely to be more severe in men than in women. 

Boston Med. and Surg. Jour., 1914, 171, 19. 


1 
2 Ann. Otol., Rhinol., and Laryngol., 1914, 23, 835, 
§ Allbutt’s System of Medicine, 5, 210, 


LARYNGEAL TUBERCULOSIS 559 


Symptoms.— These depend on the location of the lesion in the larynx. 
Those in whom the interior of the larynx is affected do not suffer as 
much as those whose trouble lies at the entrance of the larynx. The 
symptoms are few in number. Hoarseness is present in all in whom 
the interior of the larynx is affected, and it may be of various degrees, 
from mild tiring of the voice to complete aphonia. On the other hand, 
pain is more frequent when the entrance of the larynx, especially the 
epiglottis, is affected, while the voice may in these cases be retained 
quite well. ‘The pain may be spontaneous, radiating to the ear, or there 
may be a sensation of tickling which provokes cough. In advanced 
cases, with perichondritis, deep ulceration of the epiglottis, and col- 
lateral inflammatory edema of the parts, the pain may be so severe 
as to interfere with swallowing food. Usually warm fluids and solids 
cannot be passed. The dysphagia may be so severe as to prevent 





Fig. 106 —Tuberculosis of the larynx. (Ballenger.) 


swallowing altogether. I have seen some cases in which swallowing 
of saliva was more painful than that of food. Local external tenderness 
israre. Stridor, and obstruction of respiration, are comparatively rare, 
but they do occur now and then. 

Julius Dworetzky, whose experience has been immense, classifies 
the clinical course of laryngeal tuberculosis into the acute, subacute, 
and the chronic types. The least frequent is the acute type, which is 
characterized by a soft edema of the larynx with a marked tendency 
to ulceration and no tendency to fibrosis. It is usually found in far 
advanced cases, but may, on rare occasions, be met with in incipients. 
Hoarseness, a sensation of fulness in the throat, dysphagia, etc., are 
very much accentuated. The outlook is grave; nearly all patients 
succumb within a few months. The swhacute type shows a moderate 
tendency to fibrosis of the lesion. Papilliform infiltrates and_ soft 


560 COMPLICATIONS OF PHTHISIS 


polypoid excrescences are usually found laryngoscopically. When the 
true vocal cords or the interarytenoid sulcus are involved, hoarseness 
is aclinical feature of these cases. The prognosis is favorable, especially 
if proper treatment is instituted. In the chronic type the tendency to_ 





Fre. 107.—Incipient tuberculosis of the Fig. 108.—Chronic tuberculosis of the 
larynx. Infiltration of posterior com- larynx. Papillomatous infiltration of 
missure with slight thickening of aryte- the posterior half of right cord with 
noids. (Dworetzky.) slight thickening at interarytenoid space. 

(Dworetzky.) 


fibrosis and healing is strongly marked. The symptoms referable to 
the larynx are mild, or may be lacking altogether. The prognosis is 
excellent. It is this type of laryngeal tuberculosis which may exist 
for a long time without annoying the patient very much. 








Fic. 109.—Chronic tuberculosis of Fic. 110.—Marked infiltration of epiglot- 
the larynx. Left cord thickened owing tis; pear-shaped arytenoids. Infiltration and 
to tuberculous infiltration; right cord erosions of both false and true cords. 


slightly so. Shght interarytenoid (Dworetsky.) 
thickening. (Dworetzky.) 


Diagnosis.—Considering the immense prognostic significance of 
laryngeal tuberculosis, we must be guarded in making a diagnosis 
of this complication. Hoarseness alone is insufficient for a diagnosis, 


LARYNGEAL TUBERCULOSIS 561 


because it may be absent when the larynx is implicated but the vocal 
cords remain in good shape; or it may be present in a patient suffering 
from phthisis, yet no tuberculous lesion is discoverable in the larynx. 
This is seen when the right recurrent laryngeal nerve is implicated in 
a thickened right apical pleural lesion, or when the two laryngeal 
nerves are pressed upon by enlarged tracheal glands. It must also be 
borne in mind that simple chronic laryngitis and pharyngitis are 
extremely common in phthisical subjects, as has been pointed out by 
Harold S. Barwell,! and they may cause hoarseness and throat discom- 
fort. The constant coughing and the irritation of the sputum passing 
through the larynx may produce a simple laryngeal catarrh. 

W. Freudenthal? urges that lasting hoarseness, apparently due to 
simple laryngitis, and seen in a patient who is not presenting symptoms 
of alcoholism or constitutional diseases, as gout or rheumatism, should 
excite suspicion of tuberculosis. 





Fig. 111.—Far advanced tuberculosis of Fic. 112.—Erosion of right half of 
the larynx. Erosion of the entire right epiglottis and right aryepiglottidean 
vocal cord; infiltration and erosion of fold. Ulceration of right arytenoid. 
right ventricular band. ‘‘Mouse-eaten”’ (Dworetsky.) 


appearance of the left cord and hyper- 
plasia of posterior commissure; infiltra- 
tion of both arytenoids. (Dworetsky.) 


The diagnosis of tuberculous laryngitis is quite easy when there are 
ulcerations, but in the incipient stage it appears to be just as difficult 
as the diagnosis of incipient pulmonary tuberculosis. Laryngologists 
usually enumerate the laryngoscopic signs of advanced disease, evi- 
dently because they mostly see advanced cases. 

Some authors have maintained that the tuberculous larynx is char- 
acterized by pallor of the mucous membrane. But it appears that pal- 
lor alone is insufficient for a diagnosis, because the larynx shares the 
pallor of the fauces which is seen in most tuberculous patients; it is 
also found in those who suffer from severe anemia of any kind. In 
fact, there are just as many red and congested larynges in phthisical 
subjects as pale ones. 


1 Lancet, 1909, 1, 1249. 2 Ztschr. f. Tuberkulose, 1910, 16, 338. 
36 


562 COMPLICATIONS OF PHTHISIS 


Paresis of the vocal cord on the side of the lung lesion, associated 
with slight chronic laryngitis, is one of the signs of incipient tubercu- 
losis ot the larynx, according to many authors, notably F. Stern.1 He 
alls this the “larynx sign” of early pulmonary tuberculosis and advises 
direct visual inspection to detect it when there is a sensation of vague 
oppression of the chest, a tendency to rheumatic pains, slightly irreg- 
ular breathing, or gastric disturbances. The entrance to the throat 
is moderately red, and the paralyzed vocal cord is also red. There is 
always more mucus on the paretic cord than on the other, and its 
inner margin is usually irregular in outline. There is slight hoarse- 
ness, particularly at night, and the patient hawks often, but raises 
very little sputum, and tubercle bacilli may not be found at this early 
stage. 

Thickening and even ulceration of the posterior wall of the larynx 
is another early sign. Uniform redness of both vocal cords is not 
pathognomonic of tuberculosis, but when one cord is red while the 
other remains normal or is pale, tuberculosis is probably present. 

With the advance of the process the smooth and shiny appearance 
of the parts is changed owing to the ulceration. ‘The infiltration often 
affects the epiglottis, producing that pale, rounded, sausage-like body 
which may attain such dimensions as to obstruct the view of the inte- 
rior of the larynx. The arytenoid cartilages often change into pyriform 
bodies. When the infiltration begins to ulcerate, the characteristic 
worm-eaten appearance of the parts is seen, together with caries, 
perichondritis, necrosis, and exfoliation of parts of the cartilages. 

In cases in which the infiltration begins in one or both vocal cords 
or the ventricular bands, or the interarytenoid region, the prognosis 
is more favorable. However, one or both cords may be destroyed by 
ulceration. In far-advanced cases all parts may be destroyed, includ- 
ing the epiglottis, of which only a short stump may be left. 

Prognosis. — 7'he outlook in phthisis complicated by tuberculosis laryn- 
gitis is rather gloomy, though not invariably fatal, as was once thought. 
Forty years ago Morell Mackenzie stated that “it is not certain 
that any cases ever recover.” His statistics showed that it reduced 
the average expectation of life to twelve or eighteen months, very few 
patients living more than two and a half years. But since phthisis 
has decreased in malignancy during recent years, patients su!ering 
from laryngeal tuberculosis have also benefited, and we now know that 
many recover. ‘The lesion in the throat may heal, as has been found by 
careful studies of postmortem findings. St. Clair Thomson? recently 
reported a case treated twenty years ago, the patient keeping well ever 
since. 

The laryngeal lesion per se only rarely kills the patient, and it has 
been stated that “consumptives never die from the larynx.” This is 
wrong, of course, because we occasionally see a case of sudden death 


1 Berl. klin. Wehnschr., 1914, 51, 1419. 2 Tubercle, 1919, 1, 13. 


GANGRENE OF THE LUNGS 563 


from asphyxia or edema of the glottis. The bulk of the patients with 
laryngeal complication die as a result of the severity of the pulmonary 
lesion, or inanition, due to painful deglutition. In fact, when the 
larynx is extensively involved, producing dysphagia, dysphonia, etc., 
a fatal issue may be expected sooner or later. If the lesions in the lung 
and larynx are not sufficient to kill the patient he will die as a result 
of inanition. 

The milder subacute and chronic forms of laryngeal tuberculosis 
have a better outlook. Many heal spontaneously without any local 
treatment. The general treatment instituted often hastens recovery 
from the laryngeal lesion. Very often the condition of the larynx goes 
hand-in-hand with the general condition of the patient, both improving, 
or aggravating, simultaneously. Very few are benefited by local 
treatment. 

Gangrene of the Lungs.—'This is an exceedingly rare complication 
of phthisis; it is more often found in cases of bronchiectasis, especially 
in old subjects. Considering that mixed infection is very frequent in 
phthisis, although the contaminating microérganisms are not respon- 
sible for most of the symptoms of the disease, it is surprising that 
putretactive germs should but rarely take root in phthisical lungs. 
When occurring, it is soon recognized by the fetid breath and expectora- 
tion. But not all phthisical patients with fetid sputum have gangrene 
of the lung. Sputum retained in tuberculous cavities may become 
fetid. In such cases the malodorous expectoration lasts only for a few 
days or weeks, and sooner or later assumes the odor usually met in 
phthisis. Its odor also is different from that of gangrenous sputum 
—it is of a sweetish and nauseating character, while in gangrene it 
is pungent, and actually suffocating. The constitutional symptoms 
in gangrene are characteristic: The temperature rises high, the 
patient passes into a septic state with acute asthenia, and succumbs 
rapidly. In afebrile cases of phthisis a sudden rise in the temperature, 
accompanied by fetid sputum, is a sure indication of complicating 
gangrene of the lung. 

In two cases of pulmonary gangrene complicating phthisis we have 
recently found various forms of spirochete and fusiform bacilli in the 
sputum; In one case these organisms were found in the gangrenous 
tissue after the lung was removed at the necropsy of the patient. As 
was the case in spirochetal gangrene of the lung without tuberculous 
lesions! these patients suffered from pyorrhea alveolaris. There thus 
seems to be justification for the assumption that the complicating 
gangrene is due to spirochete which are carried to the lungs by aspira- 
tion, or more likely by hematogenous metastasis of the infective 
material from the gums. On the other hand, we have recently also 
found spirochete in the sputum of tuberculous patients without 
gangrene of the lungs. 


1 Fishberg and Kline: Arch. Intern. Med., 1921, 27, 61. 


564 COMPLICATIONS OF PHTHISIS 


Tuberculous Ulceration of the Intestines.— The frequency of intes- 
tinal ulcerations found at autopsies on tuberculous subjects would 
indicate that they are more frequent than they are diagnosed intra 
vitem. Thus, Louis found ulcers in five-sixths of his cases; Bayle 
and Lebert, in two-thirds; Williams found at the Brompton Hospital 
postmortems in 81 per cent intestinal ulcerations of a tuberculous 
nature; and Perey Kidd found them in 71 per cent. While they are 
responsible for the diarrhea in advanced phthisis in most cases, in 
many the looseness of the bowels is due to the toxemia, the toxic sub- 
stances in the blood being eliminated through the intestines, or swal- 
lowed sputum is the cause. Lardaceous disease of the intestines Is 
very frequently responsible, while errors in diet, especially an excess 
of fat, or of milk, and particularly raw eggs, may induce diarrhea which 
is difficult to control. 

There may be eight, ten, or even twenty, motions a day, expelling 
loose, dark, or chocolate-colored matter, exceedingly fetid, and it may 
contain small sloughs from the bowels. Quite often it is tinged with 
blood, but copious hemorrhages from the bowel are exceedingly rare. 
Kk. W. Lange,! looking for occult blood in the stools of tuberculous 
patients, found that tuberculous ulceration of the intestine may exist 
for a long time without giving rise to bleeding, and from his researches 
it appears that a negative result of a test for occult blood does not 
exclude ulceration of the intestine. John M. Cruice? says that when 
hemorrhage occurs it is of grave prognostic significance. The first case 
of this kind was reported by Tonnelle in 1829. In 1892 Guyenet could 
find only 15 cases in medical literature and Cruice found 10 additional 
cases in 1913. Although the prognosis is very grave in intestinal 
hemorrhage, L. S$. Peters, Bullock, and Bonney report cases that 
recovered. 

One characteristic of tuberculous diarrhea is its persistence. It 
may be checked by proper dietetic and medicinal treatment, but no 
sooner is this omitted than it reappears. With the diarrhea the 
emaciation proceeds at a rapid pace and they usually foreshadow 
quick relief from the suffering. I have seen patients who had been 
gaining, lose within one week all they gained in months, and within 
two to four weeks they were reduced to mere skeletons. But it must 
be mentioned that while diarrhea is a frequent symptom of tuberculous 
ulceration of the intestine, it is lacking in nearly 50 per cent of cases. 

Diagnosis. —It is very difficult to say with certainty whether the diar- 
rhea in a consumptive is due to toxemia or to intestinal ulceration. 
Tenderness is often found in the right iliac fossa, but it may be all 
over the abdomen, or any part of it. J. Walsh? made a thorough 
study of the symptomatology of intestinal ulceration, correlating 
it with autopsy findings in 100 cases at the Phipps Institute. The 


1 Ugeskrift for Laeger, 1917, 79, 1371. 
2 Medical Record, 1913, 89, 471. 
3 National Assn. Study and Prev. Tuberc., 1909, 5, 217. 


PERITONITIS 565 


usual symptoms relied on—diarrhea and abdominal pains, tender- 
ness and rigidity, especially in the region of the ileocecal valve—were 
carefully studied. He found that singly these symptoms add little 
or nothing to the diagnosis of intestinal tuberculosis, nor do any two, 
or all four when found in the same patient, because they may be 
encountered in cases in which the autopsy shows no ulcerations in the 
intestines, and the reverse. The presence of an ischiorectal abscess in 
an advanced case adds to the probability of intestinal ulcerations. 
Nor has he found any relation between the presence or absence of 
albumin or indican in the urine, or the results of the diazo-reaction, 
and intestinal ulceration. He concludes that the diagnosis of intestinal 
tuberculosis cannot be made with the slightest degree of certainty from 
our present known symptoms, and since the condition carries with it 
such an unfavorable prognosis, he advises that it is best that the 
diagnosis should not be made, so that the patient will have a better 
chance for hopeful treatment. 

During recent years some authors have urged the 2-rays in the 
diagnosis of intestinal tuberculosis. In 1912 Béclére and Mériel! 
showed that an ulcerated mucous membrane can be detected by a study 
of its motility; peristalsis was found abnormally strong, and the 
contents of the bowel were rapidly evacuated after reaching the colon. 
Similarly Stierlin? also found excessive motility of the contents of the 
colon in cases with tuberculous ulceration. Brown and Sampson, 
repeating these investigations, arrived at the conclusion that when 
in a patient with pulmonary tuberculosis the roentgenologic picture 
shows hypermotility and spasm of the colon, or filling defects, a definite 
diagnosis of colonic tuberculosis may be made. A careful investigation 
of this problem in my wards at the Montefiore Hospital has not con- 
firmed these findings. In cases with undoubted tuberculous ulceration 
of the intestines, verified by necropsy, no hypermotility of the colon or 
cecum was found, and filling defects were lacking, and the reverse. 

While the outlook for healing of these ulcers is remote, yet it is 
possible. Amenomiya‘ shows that regeneration and healing are possible 
even without scar formation, but the muscular coat is never regenerated. 

Peritonitis.—The pathogenesis of tuberculous peritonitis as a 
complication of phthisis is no more the disputed problem which it 
was formerly. Considering the frequency of bacilliemia in phthisis, 
it is clear that the blood may bring tubercle bacilli to the peritoneum 
just as readily as to other serous membranes. It is not so frequent a 
complication as is laryngeal or intestinal tuberculosis, but it appar- 
ently occurs more often than is suspected at the bedside, and we are 
at times surprised to find it at the autopsy when, intra wtam, even in 
carefully watched cases, it was not suspected. 


1 Congrés francaise de chirurgie, Paris, 1912, 25, 103. 
2 Miinchen. med. Wehnschr., 1911, 58, 1231. 

3 Jour. Am. Med. Assn., 1919, 73, 77. 

4 Virchows Archives, 1910, 201, 231. 


566 COMPLICATIONS OF PHTHISIS 


Authors disagree as to its frequency in phthisis. Munstermann! 
found it in 5 per cent of cases; Borschke’ in 16.17 per cent. In his 
autopsy material P. Horton-Smith Hartley fourd it in only 3.4 per 
cent of cases. Perforation of tuberculous ulcers of the bowels was 
observed in 3 cases out of 263 autopsies, or a percentage of 1.1, the 
perforation in each of the instances occurring in the ileum. It appears 
to be very frequent in acute miliary tuberculosis, but in chronic pul- 
monary tuberculosis it is less often encountered. While in many cases 
the infection of the peritoneum can only be explained by assuming 
that the bacilli were brought there by the blood, in a considerable 
number they may travel by way of the lymphatics from the pleura, 
the pericardium, from the mesenteric lymph glands and above all by 
contiguity from infiltrated Peyer’s patches and ulcers of the intes- 
tines. They may also come by contiguity from tuberculous lesions 
of the urogenital system, especially from the adrenals, which are often 
the seat of tuberculous changes in phthisis. 

Symptoms.— We meet mainly with two forms of this complication: 
dry, adhesive, and moist or exudative, both of which may be acute or 
chronic. During the course of phthisis the acute form, in the clinical 
sense, 1s usually due to perforation of an intestinal ulcer, or, more rarely, 
a pyothorax breaking into the peritoneal cavity, when it may produce 
suppurative peritonitis. In one case, in which during life the condition 
was not even suspected, I found at the autopsy a minute opening 
through the diaphragm permitting leakage of the pus from a pyo- 
pneumothorax. In such eases the symptoms are those of acute septic 
peritonitis... Fenwick? maintains that in some cases there may be 
premonitory symptoms, viz., pain for a few days before actual per- 
foration takes place from a tuberculous intestinal ulcer; in others 
there may be bilious vomiting, the abdomen is distended, and hyper- 
resonant on percussion. These premonitory symptoms are obviously 
due to local acute peritonitis. The actual perforation may occur dur- 
ing straining at stool, during an attack of vomiting or retching, or 
altogether while the patient is at rest. Some patients feel acute 
pain or a sensation as if something had given way in the abdomen. 
Collapse ensues and within a few hours or days the patient succumbs 
to cardiac failure. Some recuperate from the shock but they suc- 
cumb within a few days to the symptoms of acute peritonitis, or more 
rarely to exhaustion. 

The chronic form may be overlooked because it often runs its course 
symptomless. The patient may complain of abdominal pain, vomit, 
and have diarrhea, but these symptoms are very frequent during the 
course of phthisis without any peritoneal complication. On the other 
hand, there are cases with peritonitis in which these symptoms are 
lacking. The ascitic form is exceedingly rare in phthisis, though now 


1 Die Bauchfelltuberkulose, Munich, 1890. 
2 Virchows Archives, 1892, 127, 121. 
3 Dyspepsia of Phthisis, London, 1894, p. 176. 


PERITONITIS 567 


and then we meet with a case in which the abdomen is filled with 
fluid. ‘To be sure, there are many cases with exudates, but they usually 
escape detection until they assume large dimensions. 

The fluid must be considerable to be discoverable by percussion. F. 
Mueller experimented on cadavers and found that in children under 
one year of age 200 cc of fluid in the peritoneum may be discovered 
in the peritoneum by percussion. In adults only two liters gave per- 
cussion signs; 1.5 liters gave some dulness in the dependent portions, 
while 1 liter could not be detected. In the living, Mueller, Sahl, 
and others state, conditions are more favorable, because of the elas- 
ticity of the abdominal wall and viscera. Small effusions may be 
detected in the knee-chest position. In many cases the patients 
note that while the chest and extremities become extremely emaciated, 
the abdomen grows in size. 

The ascitic fluid may be serous, serofibrinous, hemorrhagic, and, 
rarely, purulent. In extremely rare instances it is found to be chylous. 
Tubercle bacilli are frequently found init. Microscopically an excess 
of lymphocytes are found. 

The adhesive form is characterized by the formation of adhesions and 
cicatricial contractions of the mesentery and gluing together of loops 
of the gut are very frequent. Especially frequent are adhesions ot the 
peritoneum to the liver and spleen. The adhesions and cicatricial 
contractions, at times, produce incomplete stenosis of the intestine 
with resultant persistent constipation and uncontrollable vomiting. 
Colicky pains, increased by pressure and on movement, may be 
observed. In these cases the emaciation may be extreme, despite 
the fact that the local lesion in the lungs is not extensive nor very 
active. When the inflammation in the peritoneum is limited and 
circumscribed, which is not infrequent, the pain may be localized 
at one point. It is noteworthy that fever may be absent, but in most 
cases of active phthisis, pyrexia due to the lung lesion is so frequent 
that it cannot be utilized for diagnostic purposes as to the presence 
or absence of a peritoneal complication. On the other hand, when the 
lesion in the lung is quiescent or latent, the complicating peritonitis 
may pass an apyretic course. In many cases there is diarrhea due to 
intestinal catarrh or, more frequently, to ulcerations of the intestine. 

As was already stated, many cases run their course painlessly. When 
copious, the exudate is easily detected by the usual physical signs 
bearing in mind that the fluid is shifting with the position of the body. 
In others it is encysted because of plastic fibrinous formation. Thor- 
mayer! described physical signs which he considers characteristic of 
tuberculous and carcinomatous peritonitis. He found that tympany 
is very frequently elicited on the right side of the abdomen, while on 
the left side a dull note is elicited by percussion. He explains this 
phenomenon on anatomical grounds: ‘The mesentery in the right 


1 Ztschr. f. klin. Med., 1884, 7, 378. 


568 COMPLICATIONS OF PHTHISIS 


side usually contracts more than in the left, and thus intestinal coils 
are apt to be drawn to the right by the shrinking mesentery; tympany 
is then elicited over these distended intestinal coils. It is, however, 
an inconstant symptom and if it occurs at all, it is discerned late, after 
the organization of the exudate. 

At times we may, on palpating the abdomen, feel some crepitation, 
and in some cases I have even heard friction sounds while auscultating 
with the stethoscope. In rare instances, tumor-like masses are 
palpable in the abdomen. When localized in the right side they may 
simulate appendicitis. In one case under my care repeated attacks of 
pain in the right lower part of the abdomen, constipation, and even 
rigidity of the rectus muscle exquisitely simulated appendictis. But 
later when a tumor was palpable the condition was cleared up. In 
another case under my care symptoms not unlike those of intestinal 
obstruction were present in a woman with tuberculous pleurisy, and 
the advisability of operative interference was seriously considered, 
but the patient recovered. It appears that tuberculous cicatrices 
causing narrowing ot the gut may stretch, and thus relief ensues. ‘This 
is also true of cicatrices of the intestinal wall caused by healing tuber- 
culous ulcers. 

Cardiac Complications.—We have shown that phthisis only excep- 
tionally develops in persons suffering from chronic endocarditis, except- 
ing in those with congenital heart disease (p. 127). But endocarditis 
may develop during the course of phthisis, either due to complicating 
rheumatic disease, or any other accidental septic process, as tonsil- 
litis, ete. The verrucose excrescences on the cardiac valves often 
found at autopsies on phthisical subjects are usually caused by other 
microérganisms, though Heller, Leyden, Benda, Tripier, and others 
maintain that tubercle bacilli may be responsible in some cases. 

Myocarditis.—In most cases heart failure in advanced phthisis is 
due to myocarditis, with dilatation of the right heart; to tuberculous 
pericarditis with adhesions to the pleura, and also to dilatation with 
‘ardiac displacement. Like in other chronic, cachectic, and exhausting 
diseases, the myocardium partakes in the atrophy of the muscular 
system and gives way from sheer exhaustion. In fibroid phthisis, 
and the pleural forms of chronic phthisis, the induration in the lungs 
interferes with the circulation, and heart failure of variable degree is 
the result. Before the onset of decompensation, hypertrophy of the 
right ventricle is quite common, especially in fibroid phthisis. 

Pulsations in the epigastrium, and accentuation of the second pul- 
monic sound reveal this condition. However, accentuation of the 
second pulmonic sound may be present without hypertrophy when 
the left lung is retracted through infiltration or shrinkage and reveals 
the left heart. ‘The constitutional symptoms of heart failure—dyspnea, 
edema, ete.—may be quite marked. 

Pericarditis.— Pericarditis may occur during the course of chronic 
phthisis. Several cases of primary tuberculous pericarditis have been 


PHLEBITIS AND THROMBOSIS 569 


reported. In chronic phthisis the pericardial sac may be implicated 
by tuberculous processes of the pleura or mediastinal glands. Adhe- 
sions between the pleura and pericardium are often found and with 
the shrinkage of the affected lung the heart is pulled out of its normal 
position, as has already been described. 

Very often we meet with acute pericarditis in phthisis and pleuro- 
pericardial friction sounds may be audible. The symptoms and signs 
characteristic of adhesive pericarditis are not rare in chronic phthisis— 
systolic retraction of the chest wall at the apex, engorgement of the 
veins in the neck, disappearance or weakening of the pulse during 
inspiration, ete. 

In very rare instances we meet with acute pericarditis coming on 
suddenly with pain in the cardiac region, dyspnea, cyanosis, cardiac 
irregularity, etc. In one case under my care the symptoms simulated 
pneumothorax. Careful examination of the heart, however, clears up 
the case. The cardiac dulness is increased, friction sounds are audible, 
the apex beat disappears with the effusion. The pericardium may 
also be implicated in cases of pneumothorax, producing pneumoperi- 
cardium, as has already been mentioned. 

Phlebitis and Thrombosis.—Although occurring quite frequently 
during the course of phthisis, phlebitis and thrombophlebitis are only 
rarely mentioned as complications of this disease. Older clinicians, 
as Hoffmann in 1740, and after him Hunter, Louis, Trousseau, and 
others have mentioned it, and Cursham wrote in 1860 on “Causes 
of Obstruction of the Veins of the Lower Extremities Causing Edema 
of the Corresponding Limb and Occurring in Phthisical Patients.” 
Most writers are inclined to attribute them to the tuberculous toxemia, 
while others have found in them an instance of marantic thrombosis. 
But Gustav Liebermeister,! in a thorough clinical and pathological 
study of the subject, attributes them to the direct action of the bacilli 
on the bloodvessels, finding as he does that nearly all tuberculous 
patients have a bacteremia. Haushalter and Etiénne, Vaquez, 
Sabrazés and Mongour, Chantemesse and Widal, Lesné and Revaut, 
Liebermeister, and others have found virulent tubercle bacilli in such 
thrombi. In cases under my care no tubercle bacilli could be found in 
the thrombi microscopically or by inoculation of animals. 

Phlebitis and thrombosis in phthisis usually occur in the femoral 
vein, though at times we meet with cases in which the vena cava, the 
innominate, jugular, subclavian, or renal veins or even the cerebral 
sinuses are affected. The frequency of this complication is given by 
P. R. Dowdell? as 30 among 1300 consumptives, or 1.5 per cent. H. 
Ruge and Hierokles? found it 19 times among 1778 cases of 
pulmonary tuberculosis, or 1 per cent. In my experience it appears 
to be even more frequent in advanced and active cases of phthisis. 


1 Virchows Archiv, 1909, 198, 332. 
2 Am. Jour. Med. Sci., 1893, 105, 641. 
3 Berl. klin. Wehnschr., 1899, 36, 73. 


570 COMPLICATIONS OF PHTHISIS 


P. Horton-Smith Hartley found thrombosis of veins in 2.6 per cent 
of 263 cases which came to autopsy. In males the percentage was 
but 1, while in females it was 6.6. [than A. Gray observed thrombo- 
phlebitis as a complication of phthisis 7 times in 1400 cases at the 
Chicago Fresh Air Hospital: 3 in men and 4 in women. 

Phlebitis is at times found in the veins of the upper or lower extremi- 
ties, especially in very active cases running high fever. Mostly the 
medium-sized or small veins are affected. Clinically, the thickening 
of the veins of the upper extremities are more easily recognized by 
palpation because of the lesser thickness of the muscles and adipose 
tissue. The affected veins are tender to the touch and also painful on 
motion of the limb. Edema of the extremities is exceptional in simple 
phlebitis, though in some cases it may occur. The phlebitis may 
disappear, to reappear again, and in most cases it is persistent till 
thrombosis also occurs, or till the fatal issue of the case. In fact, 
phlebitis 1s an ominous complication. A thrombus may develop and 
it may soften and be carried by the circulating blood to distant organs, 
producing pulmonary embolism or infarction. It may organize and 
remain as a firm, thick cord. Hirtz! described cases of phlebitis and 
thrombosis occurring during the incipient stage of phthisis, or even 
preceding the actual onset of the disease, especially in chlorotic girls. 

Thrombosis of the Femoral Veins. —'Thrombosis occurs most frequently 
in the femoral vein but, as was pointed out by Dowdell, usually the 
popliteal vein is found to contain a clot of older date, while in some 
the saphenous vein is plugged and rarely the superficial veins of the leg 
and thigh, as well as the main trunk from the tibial vein upward, are 
thrombosed. Dowdell, Ruge and Hierokles, Liebermeister, and 
others have also found thrombosis of the uterine and brachial veins, 
the prostatic plexus, and embolism of distant arteries is said to be not 
uncommon. As is the case with phlebitis, thrombosis is found mostly 
in far-advanced but acutely running cases and is usually the precursor 
of a fatal issue. 

The most important symptom is edema of the affected limb. The 
onset is usually slow and insidious, the swelling coming on gradually. 
Pain is often felt for a few days after the onset of edema, but in many 
cases this is lacking. When present it is mainly felt in the popliteal 
space where tenderness may be elicited. Inasmuch as practically all 
these patients have symptoms of active phthisis, the temperature 
is not an aid in the diagnosis—it is continuous or hectic, as the case 
may be; the onset of the thrombosis, edema, etc., has hardly any 
influence on the pyrexia. In some cases under my care there were 
disturbances in sensation of the affected limb, which was cold, numb, 
or tender. In one case the pain was excruciating and morphine alone 
was effective in relieving it in part. When the deeper veins of the 
muscles are plugged, which is not rare, there may be severe pain and 
hyperesthesia ot the calf of the affected leg. Diagnosis may be difficult 


1 Semaine Médicale, 1894, 14, 274. 


PHLEBITIS AND THROMBOSIS 571 


at first, but as soon as the edema appears, the cause is clear. In some 
cases the thrombus in the affected vein is so thick as to be palpable. 
I have many times been able to palpate the femoral and popliteal 
veins as thick, firm cords tender to the touch. 

Diagnosis.—In most cases the diagnosis of thrombosis and phlebitis 
israther easy. It is to be differentiated from edema of the extremities 
common in phthisis and due to cardiac and renal insufficiency, and 
from cachectic edema which is frequently seen in the terminal stages 
of this disease. Thrombosis always begins in one extremity and is 
confined to it, or marked on one side when fully developed. It is 
tender to the touch along the course of the veins and not necessarily 
over the edematous skin. The dilated superficial veins may at times 
contain clots. On the other hand, edema due to cardiac or renal 
disease is accompanied by signs and symptoms of these conditions, both 
lower extremities are affected by the swelling, and the tenderness along 
the course of the veins is lacking. Cachectic edema occurs on both 
sides, is painless and subsides when the patient is kept in the recum- 
bent position for some time. At times intra-abdominal pressure by 
enlarged mesenteric glands, or bands in adhesive peritonitis, on the 
common or external iliac vein, or on the femoral may produce edema 
of one extremity not unlike that of thrombosis. The same condition 
may occur, though very rarely, in the upper extremity when intratho- 
racic pressure is exerted by enlarged glands in the thorax on the main 
trunks of the veins. But careful examination will usually reveal the 
tumor or the glands which are responsible. 

Thrombosis of the Jugular Vein.—'Thrombosis causing edema of the 
upper extremity is very rare, but it does occur. Four cases have come 
under my observation. Humphrey! reported such a case in 1859; 
Lésague? observed in 1870 a case of phthisis complicated by the for- 
mation of a thrombus in the external jugular, subclavian, and humeral 
veins. Ten days after the appearance of the thrombus it was com- 
pletely softened and all symptoms of phlebitis disappeared. But 
in all other cases reported, death supervened within a couple of weeks 
after the establishment of thrombosis. The symptoms are edema, 
pain, ete., of the upper extremity. In 1904 Charles J. Aldrich’ collected 
trom the literature 9 cases of this complication of phthisis and reported 
1 of thrombosis of the left internal jugular with extension through 
the subclavian down the axillary into the basilic veins. Two weeks 
later a like thrombus appeared in the right side and extended to the 
veins of the arm. Death was due to cerebral sinus thrombosis from 
extension of the thrombus in the right internal jugular vein. In one 
of my cases thrombosis of the right internal jugular vein occurred in 
a patient with pneumothorax. 

Prognosis of Thrombosis.—The prognosis is fatal in the vast majority 
of cases because of the severity of the tuberculous process, occurring as 


1 British Med. Jour., 1859, 582, 601, 619, 650. 
2 Gaz. Méd. de Paris, 1879, 1, 649. 
3 New York Med. Jour., 1904, 79, 442. 


572 COMPLICATIONS OF PHTHISIS 


it does mainly in rapidly advancing cases of phthisis. Death may be 
due to secondary emboli which is then sudden. But I have recently 
seen several cases in which the symptoms of phlebitis and even throm- 
bosis have cleared up and the phthisical disease went on its course. 
Lésague and Ethan A. Gray have also reported cases of this character. 

Urogenital Tract.—Of other complications occurring more or less 
often during the course of phthisis may be mentioned tuberculosis 
of the urogenital tract. We have already mentioned that albuminuria 
is not uncommon in phthisis. In far-advanced cases, nephritis is 
quite frequent and we may have most of the symptoms of this 
disease, especially edema, etc., and even uremia, which is at times 
difficult to differentiate from tuberculous meningitis. In many of the 
advanced cases we may also note symptoms due to amyloid disease 
of the kidneys: Abundance of secretion of urine of low specific 
gravity containing hyaline and especially waxy casts and albumin 
in large quantities. But in this form of nephritis dropsy is infrequent. 
I have been struck with the fact that in most cases in which there is 
considerable albumin in the urine and dropsy, the temperature drops 
down to near normal and very often the activity of the process in the 
lung diminishes. The prognosis is, however, not improved. On the 
other hand, chronic nephritis, when complicated by pulmonary tuber- 
culosis has a rather favorable influence on the lung condition (see p. 
604). 

In some cases tuberculosis of the kidneys supervenes and also of the 
bladder, seminal vesicles, vas deferens, and epididymis. Tuberculosis 
of the kidneys is very difficult of diagnosis in its early stages. Finding 
acid-fast bacilli in the sediment of the urine is not sufficient to base a 
diagnosis in my experience, excepting when the specimen has been 
obtained by catheterization of the ureter. Even so there have been 
reported cases in which tubercle bacilli were found microscopically and 
by inoculation into animals, yet the autopsy, or the kidney removed by 
operation, showed no tuberculous lesion. ‘This is a fact which should 
never be lost sight of in doubtful cases. I have seen cases in which 
tubercle bacilli were thus found yet the patient improved without 
operation. Patients with tuberculous pyelitis suffer usually from 
lumbar pain of a dull character, have pus, albumin and blood, epithe- 
lium, and even caseous débris in the urine. At times there are seen 
cases in which the pain occurs in paroxysms and it is difficult of 
differentiation from that of renal colic due to stone. The reciprocal 
relations between renal and pulmonary tuberculosis are discussed else- 
where (see p. 587). 

Terminal Edema.—In a large proportion of tuberculous patients 
edema, general or local, appears a few days, or weeks, before the fatal 
termination of the case. ‘The edematous swelling is mainly seen around 
the joints of the lower extremities; but at times it involves the whole 
body. ‘The origin of this edema is not known definitely. Some are 
inclined to attribute it to nephritis, but it is met with in cases in which 
the autopsy shows that the kidneys remained in good condition. 


PURPURA 573 


Others state that it is due to myocardial degeneration, especially 
to dilatation of the right ventricle. Charles W. Mills! and John T. 
Henderson found a characteristic picture by Mosenthal’s test, with a 
marked decrease in water and sodium chloride elimination. 

Tuberculous Ulcerations of Mucous Membranes.— We have already 
pointed out that despite the fact that so much of tuberculous sputum 
passes through the mouths and lips of phthisical subjects, ulcerations 
of these parts are extremely rare. But it appears that tuberculous 
ulceration of the tongue is more frequent than is generally appreciated. 
Jame R. Scott has recently drawn attention to this fact. At the 
Montefiore Hospital I see about eight or ten cases a year. These 
ulcers may appear fissured, granulomatous, or papillomatous; in many 
cases they are located on the dorsum of the tongue but very frequently 
also on the tip, the sides and, rarely, on the frenum. I have seen some 
with ulcers of the soft palate, and very rarely on the posterior wall 
of the pharynx. Ina case under my care there were three ulcers on the 
tongue, one on the tip and two on each side. 

In most cases the diagnosis is clear, occurring as they do in patients 
with pronounced tuberculous lesions in the lungs and perhaps the 
larynx. But, at times, they may be found in a patient without very 
active symptoms of phthisis, and must then be differentiated from local 
manifestations of syphilis, carcinoma, and epithelioma. <A careful 
examination of the chest will clear up the diagnosis, because these 
ulcerations are, almost without exception, secondary to tuberculosis 
in the lung. A specimen removed and examined microscopically may 
show the characteristic tuberculous changes or tubercle bacilli. 

Purpura.—I have seen several cases of purpura hemorrhagica compli- 
cating advanced phthisis. Petechia are very frequent in many cases, 
but true purpura hemorrhagica with extensive ecchymoses scattered 
over the limbs may occur, and there may be simultaneously hemor- 
rhages from some of the mucous membranes—true purpura hemor- 
rhagica. In 3 out of the 4 cases seen by me recently there were also 
albuminuria and hematuria, and the patients succumbed shortly 
after the appearance of the purpura, and I am inclined to agree with 
John M. Cruice? to the effect that the occurrence of purpura espe- 
cially the hemorrhagic form, in the course of tuberculosis is always a 
grave symptom. 

Its etiological relation to tuberculosis is doubtful. Some authors 
are inclined to see in the tubercle bacillus a cause of the purpura, but 
the fact that it is so extremely rare in phthisical subjects shows that 
when the two diseases occur in the same subject, it is in all probability 
a coincidence. I believe that Cruice’s observation that after an 
attack of purpura physical examination will reveal a more advanced 
condition of the lesion does not at all prove that the hemorrhages into 
the skin were directly of a tuberculous character; it by no means 
excludes the chances of their being a coincidence. 





1 Am. Rev. Tuberc., 1917, 1, 573. 
2 Am. Jour. Med. Sci., 1912, 144, 875. 


574 COMPLICATIONS OF PHTHISIS 


Superficial Cold Abscesses in the Chest Wall.—Though these 
abscesses are not very uncommon in tuberculous subjects, they are only 
rarely mentioned in monographs on the subject of tuberculosis. ‘Their 
relation to phthisis was first pointed out by Leplat in 1876. Other 
French authors, notably Goujot, Duplay, Verneuil, Charvot, and others 
then described them in detail. Three varieties have been mentioned, 
one arising from the cellular tissues, one from the periosteum of the 
ribs, and a third of deep origin from the bone. Goujot described these 
abscesses as in front of the ribs, behind the ribs, and of the shirt-stud 
variety, in which a superficial and deep abscess communicates through 
an intercostal space. 

S. Souligoux, Peron, Villar, Paget, and more recently Samuel 
Robinson,! show that these abscesses are of pleuropulmonary origin. 
Robinson, with considerable a-ray experience, shows that “the time- 
worn custom of regarding such lesions as due solely to a necrotic rib is 
unquestionably a fallacy.’ Some authors state that erosion and even 
necrosis, particularly of the posterior surface of the rib, are not uncom- 
mon, but this is purely incidental. Iselin,? who studied many cases is 
of the opinion that the ribs are involved only secondarily. In.98 
operative cases, sequestra, or a probably primary bone lesion, were 
found only in 6 cases, and the ribs were involved only in 3 of them, and 
in | of these the patient had had syphilis. It usually follows old 
tuberculous pleurisy, but may be found in pulmonary cases. The 
tubercle bacilli apparently invade the chest wall through the lymphatics 
which may be found in old adhesions of the pleura. These abscesses 
have been found in rare instances, to drain by breaking through a 
tuberculous lung. ‘They are analogous to the abscesses found often 
in the vicinity of the incision for empyema of tuberculous origin. 

On the chest wall, along the line of insertion of the diaphragm, 
particularly anteriorly, or in the lower axillary region, there is noted a 
circumscribed swelling, the size of a pigeon’s or a hen’s egg, painless and 
fluctuating. I have recently seen cases in which the diameter of the 
abscess was five to six inches. ‘There is usually no surrounding inflam- 
matory induration, and only later the infected area becomes red and 
somewhat tender. When incised a moderate amount of liquid, curdy, 
pus is eliminated, but healing is slow: In most cases a fistula is left 
which persists for months; or an ulcer remains which keeps on dis- 
charging pus for a similar period. Very often the fistula or ulcer is 
located over a rib, the periosteum of which is implicated. In many 
cases healing finally takes place leaving an ugly red scar. 

The diagnosis is at times difficult—there is a question whether it 
is not an empyema pointing on the. chest wall, particularly when 
there are physical signs of a lung lesion or thick pleura elicited in the 
same area. A careful consideration of the history and course of the 
trouble, however, clears up the diagnosis. 


1 Tr. Nat. Assn., Study and Preven. of Tuberc., 1917, 13, 170. 
2 Corr.-Bl. f. schweiz. Aerzte, 1919, 49, 97. 


GHAPTER: X XX, 


RECIPROCAL RELATIONS BETWEEN PULMONARY 
- TUBERCULOSIS AND CERTAIN PHYSIOLOGICAL 
AND PATHOLOGICAL PROCESSES. 


Puumonary tuberculosis is a disease occurring at all ages and, in its 
most common form, the chronic, lasts for many years during which the 
patient is subject to the diverse physiological and pathological processes 
peculiar to mankind. Certain physiological processes, as was already 
shown elsewhere, have a great influence on the pathogenesis, course, 
and outcome of tuberculous infection and disease; others are in them- 
selves greatly affected by the tuberculous toxemia. In the long 
months, or years, during which the patient suffers from the symptoms 
of phthisis, he is liable to contract other diseases which may have an 
influence on the symptomatology and course of the lung disease; or 
conversely, the intercurrent disease may be altered in its clinical 
manifestations because of the underlying tuberculous process. These 
reciprocal relations between pulmonary tuberculosis and physiological 
and various pathological processes are of immense importance to those 
who have tuberculous patients under their care. They have great 
bearings on the origin, diagnosis, prognosis, and treatment of the 
tuberculous patient. A knowledge of these interrelations is especially 
needed by those whose practice is limited to institutions devoted exclu- 
sively to the treatment of tuberculosis, where physicians are liable to 
become “tuberculosis specialists,” oblivious of the fact that their 
patients are humans—liable to suffer from diseases other than that 
caused by the tubercle bacillus, and that an intercurrent disease may 
have an influence, at times a very favorable one, more frequently the 
reverse, on the tuberculous process. 

Growth.— Tuberculosis attacks human beings at all periods of life. 
When the disease is active during the formative age, it usually retards 
physical development, stunts growth, leaves its victim with small, 
feeble, and flabby muscles, rather slim bones, and a notoriously de- 
formed chest. As was already stated, the phthisical, or paralytic, chest 
is almost invariably the result of tuberculosis of the intrathoracic glands 
during infancy and childhood (see p. 303). It is a well-known fact 
that tuberculous children are puny, shorter than others, and weakly; 
even when they are fat, “pasty,” which is not uncommon, their 
atrophied musculature betrays trouble. It is noteworthy that many of 
these undersized children begin to grow in height after twelve or 
fourteen years of age, and may become taller than the average for their 


576 RECIPROCAL RELATIONS 


race stock. It seems that many of these tall youths present signs of 
dyspituitarism, such as prognatism, long extremeties, enlarged wrists 
and fingers, etc. Whether these changes are due to tuberculous changes 
in the pituitary, or to toxic effects on this gland, has not been 
established. It is, however, a fact commonly observed, that while 
these youths grow in height rapidly, at that age, certain secondary 
sexual characters are apt to be rather slow in their appearance; The 
axillary and pubic hair may be scanty or absent, the mammary glands 
in girls rather small, or rudimentary, menstruation delayed, ete. 
Stigmata of infantilism are common in young tuberculous subjects. 
At this age a smouldering tuberculous process in the intrathoracic 
glands is likely to flare up and invade the lungs. When this occurs, the 
prognosis is, as a rule, serious in the writer’s experience. (See p. 610). 

On the whole, it may be said that tuberculosis retards growth in 
height when attacking children under twelve years of age; it enhances 
it, when attacking adolescents between fourteen and twenty, and it 
has no effect on stature of adults in whom growth of the skeleton is an 
accomplished fact, unless it is accompanied by kyphosis or scoliosis, 
when it is reduced. Deformities of the chest occur in children as a 
result of tuberculosis; in adults they are seen to result from pleural 
adhesions and destruction of lung tissue, and manifest themselves in 
the form of flattening and localized retractions. This has been dis- 
cussed in detail in Chapter XIV. 

When judging the weight of children suspected of, or actually 
suffering from, tuberculosis the facts about growth are to be borne in 
mind. <A youth under eighteen years of age does not hold his own if 
he does not gain in weight; the gain in height should be registered on 
the scale, otherwise there is an actual loss in weight. Reports of 
institutions caring for tuberculous children at times forget this factor 
of growth, and when they indicate that their little patients had gained 
in weight, they must show that this gain has been more than could be 
accounted for by the gain in height which the children have attained 
during the given period. 

Puberty.—The interrelation between the respiratory and the genera- 
tive organs in women is more intimate that is generally appreciated. 
During menstruation and pregnancy the mucous membranes of the 
nose and larynx are very often congested, and subject to catarrhal 
changes with or without visible causes. Changes in the voice are often 
noted in women during menstruation, pregnancy, the menopause, etc. 
For centuries clinicians have noted certain influences exerted by 
tuberculous disease on ovarian function. 

A large proportion of tuberculous women, especially adolescents, 
menstruate scantily; in many complete amenorrhea occurs for months. 
Instead of the sanguineous flow, there may be merely an increase in 
the amount of mucous discharge lasting for a day or two. In fact, 
amenorrhea without any assignable cause has been considered of 
tuberculous origin by physicians and the laity; while others have 


PUBERTY 577 


considered it a cause of consumption. In a small proportion of cases 
menorrhagia or metrorrhagia is observed; in others, dysmenorrhea; 
several authors have claimed that this sort of painful menstruation may 
be relieved by proper antituberculosis treatment, especially tuberculin. 

The tuberculous woman with amenorrhea may be recognized at 
first sight in most cases. The facies of tuberculosis (see p. 299) is 
rather sharply accentuated, and pallor of the face and extremities, 
which is not very common in the average case of tuberculosis, is more 
or less severe. We have shown that the blood picture in tuberculosis 
is not characteristic (see p. 281), but in women with scanty or absent 
menstruation, a blood count of secondary anemia is the rule. 

Vicarious menstruation has been spoken of by many writers of 
former generations; hemoptysis of various degrees supplanting the 
periodical uterine flow. Careful clinical observation has, however, 
shown that in these cases we deal with ordinary tuberculous hemop- 
tysis in phthisical women in whom amenorrhea is one of the cardinal 
symptoms. In some cases there is a tuberculous lesion which has not 
been diagnosed. I have never been satisfied that any of the cases that 
came under my observation could be considered genuine vicarious 
menstruation in the sense given it by some authors. 

Menstrual hemoptysis, which has already been discussed (see p. 247), 
is observed at times. ‘The patients spit blood during the menstrual 
period, or a few days preceding it, irrespective of the effect exercised 
by the tuberculous process on the ovarian function. This goes hand 
in hand with the liability of women to suffer from acute exacerbations 
of the tuberculous lung lesion at that period, manifesting itself in 
elevation of the temperature, increase in the severity of the cough, and 
expectoration, etc. The liability to congestions of the mucous mem- 
branes of the upper respiratory tract during pregnancy may be con- 
sidered an analogous phenomenon. Similar effects of the menstrual 
function on a pathological process have been observed during the 
recent pandemics of influenza. 

When occurring in the very young, tuberculosis often hinders the 
development of the primary and secondary sexual characters. The 
infantile type of uterus is common in young tuberculous girls; hypo- 
plasia of the testicles in boys. ‘The secondary sexual characters, the 
breasts, the pubic hair (also that in the axillee) are often rudimentary, 
and the onset of menstruation may be delayed, as has already been 
noted. 

Primary tuberculosis of the generative organs is very rare, though in 
fatal pulmonary phthisis specific tuberculous changes are frequently 
found in the female pelvic organs; some authors, like Schlimpert and 
Kronig, have found this to be true in over 80 per cent of fatal cases of 
pulmonary tuberculosis. ‘This is not in agreement with the results of 
autopsies made of my own material. 

It appears that the lesions in these organs originate hematogenously, 
by metastasis from the lungs and glands. However, it seems that, 

37 


ld 
(od 


CO 


578 RECIPROCAL RELATIONS 

excepting in fatal cases of phthisis, the lungs do not show much evidence 
of active disease in patients in whom the process in the generative 
organs 1s so pronounced and disabling as to require surgical inter- 
vention. Of the many cases of surgical tuberculosis of the female 
generative organs seen by the writer, patients in whom destructive 
tuberculous lesions have been demonstrated in the organs removed 
surgically, only few showed symptoms and signs of active tuberculous 
jestonsh in the lungs. This is also to be observ ed in many cases of 
tuberculosis of the testicles. It appears to be in agreement with our 
other observations that extrathoracic tuberculous lesions shield the 
lungs against active disease (see p. 584). Several cases have been 
observed in which dormant lung lesions were reactivated soon after 
surgical operations on the generative organs for tuberculous disease. 

Sexual Function.—The popular views entertained by the laity and 
the profession to the effect that consumptives have excessive sexual 
potency and demands are apparently well founded. During the in- 
cipient stage of the disease there is often noted an increased sexual 
irritability, and this is apparently the reason why some _ believe 
that phthisis is at times due to excessive venery. Létulle asserts 
that sexual excesses are common at the commencement of the 
disease, and are checked only when the limit of exhaustion is reached. 
W. H. Peters' observed a tendency to abnormal sexual excitement so 
frequent among consumptives as to require careful attention of the 
physician. He says that ‘every physician has been impressed by the 
almost disgusting, and sometimes revolting persistence of the sexual 
instinct in consumptives, even late in the disease.” 

It is remarkable that in the advanced stages of the disease, when the 
body is extremely emaciated, the muscles atrophied and the vital 
forces apparently at their lowest, sexual potency may be retained. 
Even shortly before death a consumptive may impregnate his wife, 
and a woman who has lost half her normal weight, and is subject to 
frequent hemorrhages, runs a febrile temperature, sweats, and coughs 
distressingly, is, at times, seen in a pregnant state. Peters quotes 
Barnes, Superintendent of the Rhode Island State Sanatorium, about 
a patient who died from hemorrhage coming on during the sexual act 
which took place while on a visit from the sanatorium to his wife. I 
have met similar cases. In hospitals for advanced consumptives the 
patients must be watched in this regard, especially when the male 
division is not completely separated from the female division. Sexual 
excesses, according to Gimbert,? often hastens the fatal outcome of the 
disease. 

Wevgandt? made a collective investigation of this problem among 
physicians in German Santoriums in which incipient cases are admitted. 
Many of the answers were to the effect that they had not observed any 

1 Jour. Am. Med. Assn., 1908, 1, 9388. 


2 Rev. de la Tuberculose, 1907, 11, 1. 
3 Med. Klinik, 1912, 8, 91 and 137. 


PREGNANCY 579 


special increase in the sexual desires of their patients; three directors 
of sanatoriums, Kohler, Krause, and Marquard, sent the interesting 
information that the patients had accused the doctors of secretly 
putting aphrodisiac or anaphrodisiac drugs into the milk, or other 
food. It appears that in many German sanatoriums such superstitions 
prevail, thus indicating that the patients themselves are aware of the 
increased sexual irritability. 

These sexual excesses have been attributed to the tuberculous 
toxemia. It has also been said that the lazy, indolent life, the lack of 
muscular exercise, and the excessive consumption of nitrogenous food 
during the treatment, are more responsible for the sexual proclivities 
than the tuberculous toxemia. Some consider the association of the 
sexes In sanatoriums favors tendencies in this direction. In many 
cases the despondency engendered by the knowledge of suffering from 
an incurable disease urges the patients to take in as much of life and its 
pleasures as possible before it is too late. 

There are other chronic diseases in which the patients are idle, eat 
well and may become despondent, yet they do not indulge in sexual 
excess to the same extent as the tuberculous, which would be in line 
with the suggestion that the tuberculous toxemia is effective in the 
direction of causing sexual irritability. Turban found that in artificial 
tuberculin poisoning, 7. e., when tuberculin is administered for thera- 
peutic purposes, sexual irritability is increased, and in some cases he 
had to discard specific treatment for this reason. “Every physician 
with extensive experience with tuberculous patients,” says Muralt, 
“knows of cases in which recovery from the disease brought about 
normal functions in this regard.”’ 

Fecundation.—It is noteworthy that tuberculosis appears to have 
no influence on the function of fecundation, so long as the process in 
the lungs is not so far advanced as to render the patient completely 
bedridden. Most married tuberculous women become pregnant, 
unless measures are taken to prevent it. In fact, physicians with 
extensive experience among these patients have seen emaciated con- 
sumptive women, having fever, severe cough and profuse expectoration, 
hardly able to move about because of atrophy of the subcutaneous fat 
and muscles, become pregnant and, what is astonishing at times, they 
go on to term, and are delivered of full sized infants. Properly collated 
statistics on this point are not available, as far as the writer knows, 
because it is difficult to take into consideration the factor of prevention 
of conception, separation of the mates, etc. (See p. 298). 

Pregnancy.--Considering their vast prophylactic bearings, the 
problems of the reciprocal relations between pregnancy and tuberculous 
disease have been widely discussed, though it cannot be said that they 
have been satisfactorily studied. For centuries many physicians 
stated that they had observed that pregnancy often ameliorates the 
condition of female tuberculous patients, and some, like Cullen (1712- 
1790), recommended marriage for tuberculous girls for this reason, 


580 RECIPROCAL RELATIONS 


Dr. E. Warren,! in a prize essay published in 1857 said: “ Pregnancy, 
coition, etc., are particularly desired by women affected with phthisis, 
which constitutes a pointing of Nature toward a remedy for the evils by 
which the system has been invaded.’ He quotes the opinion of 
authorities, like Hippocrates, Sydenham, Montgomery, Parr, Roki- 
tansky, Clark, and many others, who held similar views on the effects 
of marriage and pregnancy on tuberculosis. ‘There are writers who, 
at present, speak in the same vein: Thus, Charles W. Townsend,’ 
speaking of cases observed in the Boston Lying-in Hospital, says that 

“during pregnancy the patient often seems better, and the disease 
appears in abeyance,” and that “Nature seems to put forth a supreme 
effort to suppress the disease during pregnancy and make labor easy 
and short, but after the child is born the disease advances at a rapid 
rate. A French author, Sabourin,’ is even more explicit in his recom- 
mendations of marriage for tuberculous girls because it seems to endow 
them with a certain degree of immunity and deprives them of the 

‘catamenial intoxication, the greatest enemy of tuberculous women.” 
A Spanish author, Lasbennes,! brings statistics showing that women 
of the child-bearing age have a lower mortality from tuberculosis 
than men, and concludes that matrimony is advisable for certain 
“pre-tuberculous’’ cases. 

The vast majority of modern writers are, however, opposed to these 
views, and maintain that pregnancy, labor, and lactation are liable to 
reactivate latent tuberculosis, and aggravate active lesions, often lead- 
ing to a fatal termination of otherwise favorable cases. Statistics in 
support of these contentions are not wanting. Some authors, like 
von Ysendick, Amstel, Rosthorn, and others state that this is the 
invariable outcome when a tuberculous woman becomes pregnant, 
that 100 per cent are either aggravated, or succumb; Pankow and 
Kiipferle, have found this to be the case in 95 per cent of cases; Neltner, 
Kaminer, Deibel, Felner, Schauta, Eich, Pradella, and Reiche, between 
60 and 90 per cent; Freund, in 38 per cent, while others calculated 
smaller percentages of aggravation and deaths, some even as low as 
16 per cent (Norris). Likewise, the number of deaths because of 
aggravation of the disease soon after the puerperium oscillates within 
wide limits according to published statistics. Amstel reports 100 per 
cent; Lebert, over 70 per cent; Dubel, Tesler, von Ysendick, Kiewe, 
Reiche and Kaminer, between 50 and 60 per cent; Grisolle, Pradella, 
Tecklenberg, Neltner, Rosthorn, Fellner, between 10 and 30 per cent. 

The wide divergence of these figures, running between 10 and 100 
per cent shows clearly that they are either inaccurate, or based on 
clinical material which is not comparable. It seems that those who 
reported far advanced cases had a higher proportion of aggravations 


Am. Jour. Med. Sci., 1857, 34, 87. 

Boston Med. Surg. Jour., 1897, 88, 391. 

Jour. d. Practiciens, September 6, 1918, No. 36, 
Med. Ibera, 1921, 7, 123, 


mon we 


PREGNANCY 581 


and fatalities than those who dealt with incipient, or inactive cases of 
tuberculosis. Morerecent statistics, published by internists and special- 
ists In hospitals for tuberculous patients, do not bear out the con- 
tention that pregnancy is as dangerous to all tuberculous women as the 
above figures, compiled mainly by gynecologists and obstetricians, 
would indicate. ‘Thus Norris and Landis! report of 85 cases of preg- 
nancy in tuberculous women observed at the Phipps’ Institute at 
Philadelphia during a period of five years. They found that 85 per 
cent showed no change in their condition as a result of pregnancy. 
About 20 per cent of mild, quiescent, cases of pulmonary tuberculosis, 
and 70 per cent of advanced cases showed exacerbations during 
pregnancy or the puerperium. But taking a large number of cases in 
which pregnancy does not enter into consideration, we would expect 
to find about the same percentage of aggravations during the period 
of two years which cover pregnancy and lactation. Likewise, H. J. 
Forssner’s” recently compiled statistics tend to show that the sinister 
influence of pregnancy on pulmonary tuberculosis is a dogma, a 
a tradition founded on unreliable information. He shows that exten- 
sion of the lung disease may be synchronous with, but is not neces- 
sarily dependent on, pregnancy. He found that 881 patients observed 
during the period 1907-1912 were not better off than 133 who became 
pregnant. The exacerbation of the lung disease coincided with 
pregnancy in a certain number of cases, to be sure, but inquiry shows 
that this was merely coincidental. K. Schiffer,* in a study of the after 
histories of married women discharged from a sanatorium, arrived at 
about the same conclusion. Of 425 patients thus observed during a 
period of three to eighteen years, 136 had not become pregnant, and 
189 had undergone from 1 to 7 pregnancies each since discharge. In 
76.2 per cent the women were still fit for ordinary or light work despite 
the fact that they had been pregnant and gave birth to and raised 
children; only 18.4 per cent had died of tuberculosis, but only in 13.7 
per cent was death due to the progress of the disease in connection with 
pregnancy. An examination of the after-histories showed that in the 
first stage 87 per cent, in the second, 83.3 per cent, and in the third, 
63.6 per cent were still fit for work. Compared with 236 women who 
had left the sanatorium, and had not subsequently become pregnant, 
it appears that the former were better off. Only 53.9 per cent of the 
latter were fit for work and 38.4 per cent had died, as against 76.2 and 
18.4 per cent respectively among those who had become pregnant. 
The author suggests that the non-pregnant fared worse because there 
were more far advanced cases among them. It may be added that, for 
this very reason, they may also have prevented pregnancy more 
assiduously than the others. 

It has also been repeatedly stated that pregnancy seems to engender 


1 Ann. Rep. Phipps Inst., 1918, 14, 1. 
2 Tubercle, 1920, 1, 509. 
3 Tbid., p. 515. 


582 RECIPROCAL RELATIONS 


tuberculosis in women “predisposed” to the disease. This is based on 
the statements of many patients to the effect that they had felt well 
until they conceived, and that during pregnancy, or soon after the 
puerperium, symptoms of phthisis made their appearance. Careful 
inquiry into these cases reveals the fact that many had been coughing 
for months or years before becoming pregnant, and inasmuch as 
15 to 20 per cent of tuberculous individuals are likely to suffer aggrava- 
tion in their disease during any year or two, the pregnant women appear 
not to be an exception. ‘‘ Pregnancy and the puerperium, even when 
repeatedly occurring, are well and fairly well borne by a much larger 
proportion of tuberculous women than some pessimistic physicians 
claim,” says Friedrich Kraus.!. “In general it may be confidently 
stated that tuberculous disease with mild symptoms, which dces not 
progress, the so-called ‘quiescent’ cases, which constitute about 90 
per cent of all cases, suffer no aggravation of the disease as a result of 
pregnancy, labor, or the puerperium. ‘The same is also true of about 
one-half of the number of active tuberculosis.” Of course, it is dif- 
ferent with patients in whom the disease is active and progressive, 
running fever, are emaciated and weakly, and especially those who have 

lary npéal and intestinal complications. This is the class that suecumbs 
soon after childbirth. It is, however, noteworthy that it is extremely 
rare that a tuberculous woman should die with the fetus in utero. 
I have seen numerous pregnant women with far advanced and pro- 
gressive lesions go through the long months of pregnancy, and die 
soon after the infant is expelled, but I have not seen one die before 
delivery. Moreover, there is no doubt that many tuberculous women 
feel much better, the symptoms of the disease abating to some extent, 
during pregnancy. Per haps an explanation may be found in the 
circulatory changes occurring during pregnancy. It is well known that 
the mucous membranes of the respiratory tract are congested during 
that period, and this may retard the progress of the tuberculous process 
for the time being, as is seen to be the result of pulmonary congestion 
in cases of mitral stenosis (see p. 127). 

Labor.— Many writers have suggested that the process of childbirth 
is predisposing to the evolution of phthisis and for this reason women 
who feel quite well during pregnancy develop active disease during, or 
soon after, the puerperium. Because of the straining at labor the 
intrathoracic pressure increases; in some cases to such an extent as to 
produce interstitial emphysema, in rare instances extending to the 
subcutaneous tissues of the neck. But this occurs only in extremely 
rare instances, and cannot be considered a strong predisposing factor. 
We have seen that quite often tubercle bacilli are found in the placenta 
(see p. LOS). While separating from the uterus the sinuses are opened 
and tubercle bacilli may thus gain an entrance into the general circula- 
tion and cause a bacteremia. Also, as has been suggested by Hanau, 


1 Handbuch d. Tuberkulose, 3, 280. 


THE NEWBORN INFANT 583 


after labor the diaphragm descends and thus favors aspiration of 
tuberculous material from the upper parts of the lungs to the lower. 
But we have seen while discussing phthisiogenesis (see p. 151) that in 
tuberculosis metastasis does not, and there are indications that it 
cannot, take place in this manner. Nor can anemia, due to loss of 
blood during labor, be considered predisposing. The estimated amount 
of blood lost during normal labor is between 300 and 500 grams, and 
experience has shown that it soon regenerates through excessive work 
of the hematopoietic organs. 

Experience has shown that only in cases of tuberculosis with active 
symptoms does progression downward follow pregnaney and labor. 
Those with latent, and many with quiescent lesions, pass through these 
processes unscathed. Obstetricians agree that difficult labor, involving 
manual or instrumental extraction of the fetus, does not occur more 
often than in non-tuberculous women. It is, indeed, often amazing to 
witness an emaciated, and evidently feeble woman pass through labor 
as easily as the average woman. Women who date back the onset of 
tuberculous disease to pregnancy, labor, and the puerperium are not 
much more numerous than might be expected when we bear in mind 
that a certain number of quiescent cases will reactivate within any 
given period. Perhaps the fact that during the child-bearing age, 
between fifteen and forty-five, the tuberculosis mortality is lower 
among women than among men of the same age period, shows best that 
the deletrious effects of pregnancy and labor have been exaggerated by 
some authors. 

The Newborn Infant.—While congenital tuberculosis occurs, it is 
extremely rare (see p. 108); most of the infants born to tuberculous 
mothers are free from this disease at birth. To be sure, they are soon 
infected by the mothers, and the mortality among them is appalling, 
but even so, not an inconsiderable number have good chances of 
survival. Thus, of the infants born to tuberculous mothers observed 
during a five year period at the Phipps Institute in Philadelphia, 
Norris and Landis report that 14 were dead and 65 alive. They were 
found not unusually weak at birth, and the comparatively high death 
rate was due, not so much to weakness at birth, as to bottle feeding, 
and lack of care which an infant with a healthy mother enjoys. 
Schiffer reports on the fate of children born to tuberculous mothers 
under observation for three to eighteen years. Out of 356 pregnancies, 
294 gave birth to live infants of whom 81.9 per cent had been, and still 
were, perfectly well. Of the remainder, 8.8 per cent were suffering 
from, or had died of, tuberculosis. Forssner reports his dispensary 
material among which he investigated the fate of 183 children who were 
healthy at birth and whose mothers suffered from pulmonary tubercu- 
losis at the time of birth. During an observation period of twelve 
months to nine years, 64 per cent of these infants were alive and well, 
13 per cent were tuberculous, and 25 per cent had died. But in only 
13 per cent was death certified as due to tuberculosis. In another 


im 


584 RECIPROCAL RELATIONS 


group of cases, consisting of 283 infants, born to the same mothers, but 
before they began to attend tuberculosis dispensaries, it was found that 
in November, 1917, 73 per cent were alive and well, 19 per cent were 
tuberculous, and 8 per cent had died. Of 127 infants born to tuber- 
culous mothers, 100 were cared for at home, 27 away from home. Of 
the “home” children, 67 per cent were alive and well, and 33 per cent 
had died. of, or were suffering from, tuberculosis. Of the children 
cared for away from home, 89 per cent well, and only 11 per cent 
tuberculous. 

It thus appears that, while the chances of contracting tuberculosis 
during the first few years of life are very great in infants born to 
tuberculous mothers, yet they are not all doomed. ‘This is a very 
important point in prophylaxis, to which we shall return later on. 

Extra-pulmonary Tuberculous Lesions.—It has been a time-honored 
custom of physicians to render a serious prognosis in cases of pul- 
monary tuberculosis when signs and symptoms of tuberculous lesions, 
past or present, of other organs are discovered. In “‘suspects,” and in 
borderline cases, when there are noted scars indicating healed tuber- — 
culous lesion of the skin, glands, bones, or joints, or of active disease 
of these structures, the diagnosis of pulmonary tuberculosis is made 
without the positive proof which is exacted in persons in whom these 
stigmata are wanting. We have already shown that the prognosis 1n 
phthisis is no more serious in those with such scars than in those lacking 
them. But here we want to emphasize that there seems to be a distinct 
antagonism between tuberculosis of the lungs and that of other organs 
which is not appreciated to the extent it deserves; its diagnostic and 
prognostic significance cannot be overestimated. 

Tuberculous Skin Lesions.—In sanatoriums and hospitals for 
tuberculous patients lupus, or any other tuberculous skin lesion, is 
extremely rare. In my hospital work it has been my experience that 
patients with tuberculous skin lesions only rarely have active lung 
lesions; when changes are discovered by physical exploration or roent- 
genography of the chest, the lesions are almost invariably latent, or 
healed; tubercle bacilli in the sputum are extremely rare in these cases. 
This fact has been established clinically and statistically by various 
authors, notably Jadassohn! Forchammer,? Lenglet,? Lewandowsky,’ 
Bollog, and many others. Our present views of immunity may 
explain this phenomenon: The lung lesion apparently endows the 
body with resistance against reinfection with the same virus. It is 
probably for this reason that, notwithstanding that tuberculous 
patients soil their hands, and other parts of their bodies, with sputum 
containing virulent tubercle bacilli, and at times sputum is deposited 


1 Die Tuberkulose d. Haut, 1914, p. 303. 

2 Arch. f. Dermatol. u. Syphilis, 1908, 92, 3. 
3 La Pratique Dermatol., Paris, 1902, 3, 239. 
4 Die Tuberkulose der Haut, Berlin, 1916, 64. 
5 Schweitz. med. Wehnschr., 1920, 1, 939. 


TUBERCULOUS SKIN LESIONS 585 


on open wounds of the skin, these organisms, as a rule, cannot gain a 
foothold and only rarely produce a lesion at the point of inoculation. 
Even when this does occur, as we see at times, there results a very 
benign process, akin to the “butcher’s” or “pathologist’s”” warts; it 
remains local and does not implicate the regional lymphatic glands. 
In very rare instances we see real tuberculosis verrucosa cutis on the 
fingers of tuberculous patients. It appears that a similar antagonism 
exists between visceral and skin lesions in syphilis. 

While tuberculous skin lesions are only rarely found in phthisical 
patients, it seems that the reverse does not hold to the same extent. 
Many patients have demonstrable tuberculous lesions in the lungs. 
But in most cases they are latent, or at most of a quiescent type, 
giving but little if any trouble. Jadassohn, John H. Stokes,! and 
many others, found that the lungs lesions in their tuberculous patients 
were benign. Lewandowsky suggests that while an active lung lesion 
may endow the body with a sufficiency of antibodies to prevent reinfec- 
tion, a skin lesion cannot do it, because the skin does not offer a very 
good soil for the growth of tubercle bacilli (see p. 45). Another 
plausible explanation may be the following: Lupus begins mainly in 
children under twelve vears of age. Among them pulmonary tuber- 
culosis is very rare. When these children reach maturity, the dor- 
mant lung lesions may reactivate and produce symptoms. But 
Bollog found this not to be true among 400 patients with tuberculous 
skin lesions. However, it appears that, even so, the lung lesions are, 
as a rule, rather benign in individuals with lupus. 

I have observed that in a few cases when the tuberculous skin lesions 
healed, pulmonary tuberculosis was not slow in making its appearance. 
The course of the disease in the lungs was acute and progressive. 
Recently a case of extensive lupus over the face, chest and arms was 
seen In which a very active lung disease developed. 

There is one skin disease which is frequently associated with tuber- 
culosis, especially miliary tuberculosis. I refer to erythema nodosum. 
However, it appears that only few investigators have found a tuber- 
culous bacteriemia, or even tubercle bacilli in the skin lesions of erythema 
nodosum, while most others have failed to find them. From the 
extensive literature on the subject, which may be gleaned from the 
recent works of Lewandowsky,’ Foerster,’ and Stokes,‘ it appears that 
the relations of erythema nodosum to tuberculosis have not been firmly 
established. An attack of erythema nodosum, or the presence of 
tuberculides on the skin of infants and children, by no means implies 
that the child will succumb to acute miliary tuberculosis, and the 
writer has seen cases in adults running their course within a few weeks, 
without the subsequent development of pulmonary tuberculosis. Of 


1 Am. Jour. Med. Sci., 1919, 157, 313. 

2 Die Tuberkulose der Haut, p. 212. 

3 Jour. Am. Med. Assn., 1914, 63, 1266. 

4 Arch. Dermatol. and Syphilis, 1921, 3, 29. 


586 RECIPROCAL RELATIONS 


course, this does not exclude the possibility that erythema nodosum 
is caused by a tuberculous bacteremia. 

Osseous and Articular Tuberculosis.—The vast majority of persons 
who present stigmata of glandular, osseous, and articular tuberculosis 
during childhood pass through life without developing pulmonary 
tuberculosis. On the other hand, it is exceedingly rare that a patient 
with an active lung lesion should develop a tuberculous lesion of a bone 
or joint. In patients with Pott’s disease, or with ankylosed joints, 
pulmonary tuberculosis of an active and progressive type is rare. On 
this point many statistical investigations have been made, Wang! 
found among 2000 cases of clinical pulmonary tuberculosis only 20 
with old cervical scars due to tuberculous lesions which had occurred 
during childhood. He observed that patients with such scars show a 
strong tendency to improve with the usual sanatorium treatment. 
Wallgren? observed the rarity of lung lesions in persons with old scars 
and the benign forms of pulmonary tuberculosis when it occurs in 
rare instances. [hasberg® reports that tuberculosis limited to the 
lymphatic glands, bones and joints, during childhood tends to complete 
recovery. Nearly every patient with pulmonary tuberculosis admitted 
tothe Montefiore Hospital during the past twelve years with either active 
or healed osseous, or articular tuberculosis was found to have healed, 
or quiescent, lung lesions, and when, in rare instances, the lung lesion 
was active, the progress of the disease was extremely chronic, tending 
to recovery. Demonstrable tubercle bacilli in the sputum are very 
rare. 

An important exception is to be mentioned. These extra-thoracic 
tuberculous lesions appear to shield the lungs as long as the osseous or 
articular foci are not interfered with by surgical intervention. Soon 
after an operation the patient, very frequently, is attacked by acute 
and progressive tuberculosis in any of its forms, and succumbs. In 
others, after a long standing sinus has been healed by surgery, there 
appear symptoms of active pulmonary tuberculosis. This observation 
has been made by the writer repeatedly and for this reason a great deal 
of hesitation is indulged in before surgical intervention is advised in 
extra-thoracic tuberculosis. Most experienced surgeons also urge 
conservative treatment because the final results are much better. 

Another striking confirmation of the immunity of the lung in extra- 
thoracic tuberculosis is often observed in families which are thoroughly 
tuberculized, and every child is attacked by some form of the disease. 
Those who develop glandular tuberculosis during childhood pass 
through life without lung lesions. W. Williams‘ puts it tersely in this 
fashion: ‘‘A very constant, if not invariable, fact I have observed in 
my fifty years’ experience of tuberculosis is that those members of 


Jour. Am. Med. Assn., 1917, 68, 1963. 
Upsala Liikaref6rennings, 1918, 23, 1. 
Jahrb. f. Kinderheilk., 1919, 39, 77. 
British Med. Jour., 1921, 1, 158. 


es on = 


GENITO-URINARY TUBERCULOSIS 587 


families with an inherited predisposition to the disease who suffer from 
cervical gland lesion leading to suppuration do not get pulmonary 
tuberculosis, or, indeed any other form of the malady; whereas several 
other members of the same families without gland lesions, and often 
more robust individuals, frequently develop consumption. All my 
cases have also shown signs that the apex of the corresponding lung 
had been affected but had recovered.” Wallgren made the same 
observation. This has also been confirmed by observations during the 
World War. Several authors, notably Hayek,! found that A 
showing no stigmata of past tuberculosis were more prone to develop 
pulmonary tuberculosis of a fulminating type, while those who had 
many signs of “ predisposition”’ to the disease either escaped, or, when 
attacked, suffered from intensely chronic forms of pulmonary phthisis. 

Genito-urinary Tuberculosis.—In patients with chronic pulmonary 
tuberculosis the kidneys are affected by the same process in about 
15 per cent of cases. Among 128 autopsies of my cases we found that 
22 showed tuberculous lesions of the kidneys; 8 were more or less severe 

caseous lesions and 14 miliary. In other words, the kidneys are most 
likely to be implicated in acute miliary tuberculosis which is so often a 
terminal phenomenon in chronic phthisis. It appears that as long as 
the lung lesion is active, excepting, of course, miliary cases, the lesion 
in the kidneys is in abeyance. On the other hand, most cases of so- 
called primary tuberculosis of the kidneys have very few symptoms and 
signs of active disease of the lungs. Here again operative interference 
is often followed by symptoms and signs of acute and progressive 
pulmonary tuberculosis. 

It is well known that the epididymis and seminal vesicles are very 
prone to tuberculous changes, especially after slight injuries. In some, 
though not in as many as might be expected, these organs are found 
tuberculous in patients with long-standing and pronounced lung lesions. 
But in many others, the disease of the epididymis is apparently primary, 
inasmuch as no symptoms or signs of active lung disease can be dis- 
covered. It is important to remember that these patients do fairly 
well as regards their general health. [or years the testicles may be 
swollen, tender, and annoying sinuses may be discharging. But they 
keep on gaining in weight, and acquire some of the stigmata of 
eunuchism: They become obese, listless, lazy, apathetic, and the 
secondary sexual characters become modified. In these patients cough, 
due to any cause, is at once attributed to pulmonary tuberculosis and 
proper treatment for this disease is instituted. But in most cases this 
is an error: Active and progressive pulmonary tuberculosis is rare 
among them. 

It is important to emphasize that operative interference, which is 
only rarely successful in these cases, may be instrumental in reactiva- 
ting the dormant lesions in the lungs which nearly a! undoubtedly have. 


1 Miinchen. med. Wehnschr., 1919, 66, 1316. 


588 RECIPROCAL RELATIONS 


Another fact is that patients with tuberculosis of the male generative 
organs are more apt to succumb to tuberculous meningitis than those 
with lesions in other organs. MM. Simmonds! found that fully one-third 
of 200 patients under his care died in this manner, while hardly 5 per 
cent of patients suffering from pulmonary tuberculosis succumb to 
meningeal complications. He also states that in 50 per cent of patients 
with tuberculous meningitis lesions in the generative organs may be 
found at the necropsies. ‘This is especially true of tuberculosis of the 
seminal vesicles. 

Diseases of the Respiratory Tract.—The Tonsils.—Hypertrophied 
tonsils, especially the lingual and the pharyngeal, are at present 
considered manifestations of the lymphatic diathesis. The extreme 
form of this constitution, the status thymico-lymphaticus, is compara- 
tively rare, and may be left out of consideration. But hypertrophied 
tonsils and adenoids vegetations are very common, especially during 
childhood. In children with hyperplasia of the lymphoid ring in the 
throat, the cervical and at times the tracheo-bronchial glands are very 
often enlarged. These little patients cough, have fever at irregular 
intervals, and discharge mucopurulent material from the throat and 
nose; they are ‘“‘subject to colds.’’ Because of these symptoms, a 
diagnosis of tuberculosis is very often made in these lymphatic children; 
inasmuch as they present many of the stigmata of scrofula, they are at 
least classed among the strongly predisposed. Likewise, adults with 
hypertrophy of the tonsils, because of the well known symptoms they 
present, are often treated in the same manner. 

We are begining to realize at present that lymphatism is distinctly 
antagonistic to active and progressive tuberculous disease of the lungs. 
Autopsies made by Bartel,? Symmers,*? Emerson,t Ewing,® and others, 
have shown that active tuberculosis is rare in individuals of the 
lymphatic diathesis. Clinically we find that children, as well as adults 
with large tonsils, particularly with hyperplasia of the lingual and 
pharyngeal tonsils, only rarely develop pulmonary tuberculosis. 
Indeed, it appears that patients with active and progressive tuber- 
culosis, as a rule, have small tonsils, and hardly ever adenoids. More- 
over when in a case of mild tuberculous disease of the lungs the tonsils 
are removed surgically, the result is often that the lung lesion soon 
assumes an acute and progressive character; especially the larynx is 
liable to become implicated in the tuberculous process soon after the 
operation. 

It is interesting in this connection that tuberculous patients only 
rarely suffer from the acute and epidemic infections of the nose and 
throat. Those with mild lung lesions are at times so affected, but 

1 Beitr. z. Klinik d. Tuberkul., 1915, 33, 35. 

2 Status thymico-lymphaticus, Vienna, 1912; Pathogenese der Tuberkulose, Berlin, 

Roe 
“eae, Jour. Med. Sci., 1918, 156, 40. 


4 Arch. Int. Med., 1918, 18, 169. 
5 Jour. Am. Med. Assn., 1918, 71, 1525. 


DISEASES OF THE RESPIRATORY TRACT 589 


those with acute or chronic progressive phthisis usually escape when 
other members of their families, or when the personnel of the sanatorium 
are stricken one after another. Even when affected, the acute coryza 
runs a mild course, hardly inconveniencing the patient. Clinical 
experience has taught that it is extremely rare that phthisis should 
begin with manifestations of an acute inflammatory process of the nose 
and throat. If we are satisfied that these were the first symptoms, we 
may safely exclude tuberculosis in doubtful cases. 

Diseases of the Bronchi.—The acute and chronic forms of bronchitis 
have hardly anything to do with pulmonary tuberculosis etiologically. 
In its chronic forms, bronchitis is, as a rule, secondary to cardiac or 
renal disease, or to pulmonary emphysema. While it is at times 
convenient to maintain that a case which had been treated for bron- 
chitis and the patient is indiscreet enough to have a pulmonary hemor- 
rhage, or to begin to run fever, have nightsweats, etc., that the bron- 
chitis has “turned into consumption,” it is nevertheless a fact that 
such is hardly ever the case. Nor is there anything to the commonly 
accepted notion of tuberculosis having its origin in a “neglected cold.” 
When the exciting cause of active tuberculous disease is exposure, 
the initial symptoms are those of pleurisy, or of tuberculosis with a 
localized lesion in the lung. 

Chronic bronchitis, with cough for many years, with profuse expec- 
toration, etc., hardly ever becomes tuberculous, and some authors have 
spoken of an antagonism between these two diseases. This is especially 
true of bronchiectasis. In a study of 40 cases of bronchiectasis Barth! 
found only in 1 the coexistence of tuberculosis, and he concluded that 
the two conditions are incompatible, a fact which Cruveilhier and 
Bamberger had observed before. The vast majority of cases under my 
care have not become tuberculous, though recently one who had been 
at the Montefiore Hospital for eighteen years with multiple bron- 
chiectasis, with periodical profuse and threatening pulmonary hemor- 
rhages, has suddenly, without any assignable cause, shown numerous 
tubercle bacilli in the sputum. 

Chronic pulmonary tuberculosis is at times complicated by non- 
tuberculous bronchitis, and dilatations of the bronchi are found in 
many cases of fibroid phthisis that come to autopsy. Likewise, after 
attacks of influenza, tuberculous patients may remain with symptoms 
and signs of acute, or subacute, bronchitis which clears up sooner or 
later. In intensely chronic cases of phthisis with passive congestion 
of the lungs due to cardiac decompensation, chronic bronchitis 1s very 
frequent. 

Asthma.— Many writers have stated that asthma and pulmonary 
tuberculosis are mutually exclusive, while others have maintained 
that the reverse is true. Considering asthma as a symptom, there is 
no doubt that it does occur in many cases of tuberculosis, especially 


1 In Herard, Cornil and Hanot’s La Phtisie pulmonaire, Paris, 1888, p. 359. 


590 RECIPROCAL RELATIONS 


the form known as fibroid phthisis. But carefully analyzing the 
difficulties in breathing met with in phthisis, it is clear that they are 
only rarely of the character seen in bronchial or essential asthma. 
The best appellation of the dyspnea in some cases of tuberculosis is 
that they are “ pseudo-asthmatiec.” 

It is noteworthy that when an asthmatic becomes tuberculous, 
which occurs only rarely, the paroxysmal attacks of dyspnea disappear, 
or are ameliorated. Overexertion is not, as a rule, a cause of dyspnea 
in bronchial asthma when there is no high-grade pulmonary emphy- 
sema with cardiac dilatation, as is attested by its nocturnal occurrence; 
itisinfibroid phthisis. On the other hand, afebrile tuberculous patients 
with nocturnal attacks of dyspnea, or with dyspnea on exertion, have a 
good prognosis as regards duration of life. Whilethe pseudo-asthmatic 
attacks in phthisis are usually due to pulmonary fibrosis and cardiac 
dilatation, Bezancon and de Jong! have recently shown that they may 
also be caused by anaphylaxis, as is the case in many forms of bronchial 
asthma. However, it appears that juvenile asthma has nothing to do 
with tuberculosis. The crystals, spirals, and eosinophile cells are 
almost invariably found in asthmatic sputum; they are lacking in 
tuberculous sputum, excepting eosinophiles, which are now and then 
seen is phthisis. 

Pulmonary Emphysema.—Compensatory emphysema of the un- 
affected portions of the lungs occurs in nearly all cases of chronic 
tuberculosis in which there is extensive destruction of the parenchyma. 
But this is of a vicarious nature. On the other hand, persons with 
atrophic emphysema only rarely become tuberculous, as has been 
pointed out long ago by Rokitansky. The following has been offered 
as an explanation as to why an atrophic lung is a poor soil for tubercle 
bacilli: Tuberculosis occurs mainly in individuals between eighteen 
and forty-five years of age, while pulmonary emphysema is a disease 
of persons over forty. And it is among persons of advanced age that 
we actually find the two diseases combined. However, the emphyse- 
matous form of fibroid phthisis, as well as phthisis in the aged, run an 
intensely chronic course, without fever, and with slight cough and 
expectoration; but dyspnea and cyanosis are very common in the last 
stages. The diagnosis is at times very difficult because the large 
emphysematous lung screens the tuberculous lesion to an extent as 
to render physical examination, and often roentgenography, of little 
value in attempts at localization of the lesion. In many cases only 
positive sputum decides, but in a large proportion it is negative. 

Pneumonia.—'Tuberculous patients only rarely develop genuine 
lobar pneumonia, and during epidemics of influenza the characteristic 
bronchopneumonia occurs only in comparatively few of those who 
have active tuberculous lung lesions. Now and then we meet with 
a case of true lobar pneumonia in a tuberculous patient. The symp- 


1 Presse Méd., 1920, p. 885. 


DISEASES OF THE RESPIRATORY TRACT 591 


toms are about the same as in others, with sudden onset, chill, fever, 
pain in the chest, etc. The character of the expectoration often changes 
into the rusty, viscid material characteristic of pneumonia. It is 
noteworthy that the course does not materially differ from the usual, 
the crisis occurring in seven to twelve days (see Fig. 113), and when 
termination is by lysis, the cause is usually to be sought in the activity 
of the tuberculous lesion, or in complicating empyema. 

It has been our experience that in most instances the lower lobe was 
affected and physical signs of consolidation are easily made out; 
rarely apical involvement is observed, and then differentiation from 

caseous pneumonia is extremely difficult. Bacteriological and _ sero- 
logical tests are not of great value because both or ganisms, tubercle 
bacilli and pneumococci, may be found in the sputum in either case. 
The most experienced clinician may be deceived, diagnosing an exten- 
sion of the tuberculous process in the lungs, or caseous pneumonia, 
and render an unfavorable prognosis to be astonished when, within a 
week or ten days, the temperature drops by crisis, and the patient goes 
on with his phthisis. 


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Fig. 113.—Temperature curve in a case of lobar pneumonia complicating pulmonary 
tuberculosis. 


Bronchopneumonia occurring in tuberculous patients is almost 
invariably of a caseous nature and should be considered an ill omen. 
An exception is influenzal bronchopneumonia which, as a rule, runs a 
less severe course in the tuberculous than in those who were healthy 
before the onset of the epidemic disease. But tuberculous patients 
are often left with signs and symptoms indicating involvement of new 
areas of lung tissue. However, these newly involved areas, in many 
cases, clear up sooner or later, while the tuberculous lesion keeps on its 
course as if no complication had occurred. 

On the other hand, the prognosis of lobar pneumonia in tuberculous 
patients is rather favorable. Most patients recover and no trace is 
left behind, the phthisical process pursuing its course as might be 
expected. This was already noted by Walshe who said: “If lungs, 
already tuberculized, become acutely inflamed, convalescence from the 
pneumonia often takes place as rapidly, as if the lungs had previously 
been sound; and no increase in activity of the tuberculous disease 


592 RECIPROCAL RELATIONS 
necessarily follows.” Grisolle, Wilson Fox, and many others, also 
found that pneumonia exerts little or no influence on the course of 
phthisis. Some writers have even maintained that the pneumonia 
process has a rather salutary effect on the tuberculous lesion. ‘Thus, 
W. J. Pettit! arrives at the conclusion that intercurrent pneumonia 
during the course of phthisis is not unfavorable, but appears to have 
been an important factor in the production of a cure. He compares 
it with the effects of erysipelas which has repeatedly been observed to 
cure chronic indolent tuberculous ulcers, and he is inclined to assume 
that a similar reaction occurs in the lungs. Ernst v. Czyhlar? has 
made similar observations. 

There remains yet to mention the fact that lobar pneumonia is 
hardly every followed by pulmonary tuberculosis. The residual lung 
lesions after lobar and bronchopneumonia are abscess and, rarely 
gangrene of the lung, chronic intersititial pneumonia, with or without 
the formation of bronchiectasis, or localized chronic bronchitis. ‘The 
last is especially apt to follow influenzal pneumonia. In most cases 
which are considered as “unresolved pneumonia’’ it is found that the 
lesion is a localized or encapsulated empyema, but tuberculosis is 
exceedingly rare. To be sure, many tuberculous patients give a 
history of pneumonia at the beginning of their malady. But an 
investigation, whenever possible, usually reveals that an acute onset 
of pulmonary tuberculosis was mistaken for pneumonia. 

Diseases of the Circulatory Organs.—The organs of circulation are 
affected by tuberculosis in two ways, wv2., by the toxic effects, and 
mechanically. The toxemia of phthisis is effective in producing 
hypotension, tachycardia, and instability of the pulse-rate. In cases 
in which the toxic action is prolonged and intense, myocarditis is the 
rule; in the milder cases cardiac neuroses, and instability of the vaso- 
motor functions are noted. ‘These effects may be seen in early cases. 
They may disappear with the decline or disappearance of the fever. 

With the advance of the disease, when destruction of pulmonary 
tissues has gone quite far, mechanical effects manifest themselves in 
the heart and bloodvessels. This is especially seen in fibroid phthisis 
in which the cardiac symptoms may prove more annoying than those 
resulting from the tuberculous process per se, and the toxemia, which 
is lacking in many cases. Because of the obliteration of many pul- 
monary bloodvessels, the heart finds difficulty in propelling sufficient 
blood to the systemic circulation. The result is enlargement and 
dilatation of the right heart, and stasis in the veins. Many authors 
notably Regnault,? Bohland,! Sokolowski,> and many others, speak of 
hypertrophy and dilatation of the right heart in chronic cases of 


Jour. Am. Med. Assn., 1912, 58, 852. 
Beitr. z. Klin. d. Tuberkulose, 1911, 21, 33. 
Le coeur chez les tuberculeux, Paris, 1899. 
Handbuch d. Tuberkulose, 4, p. 5. 

Arch. f. klin. Med., 1885, 27, 443. 


om Ow eH 


DISEASE OF THE CIRCULATORY ORGANS 593 


tuberculosis. But a careful study by modern methods made by Boas. 
and Mann! of material at the Montefiore Hospital showed that with 
the aid of electrocardiography right ventricular predominance is not 
found more frequently in association with fibroid phthisis, or with 
pleural adhesions, than with other types of pulmonary tuberculosis. 
In fact, autopsy experience shows that a large heart is very rare in 
fatal cases of pulmonary tuberculosis. 

Clinically it is, at times, difficult to determine with exactitude 
whether the dyspnea, acrocyanosis, edema, enlargement of the visceral 
organs, notably the liver, are of cardiac or pulmonary origin. One 
of the most convenient ways to solve this problem is to put the patient 
to bed at perfect rest for a week or two. If this is effective in reducing 
the rate of the pulse, ameliorate the dyspnea, etc., it is clear that the 
heart is, in a great measure, responsible. However, in toxic myo- 
carditis rest, instrumental in reducing the toxemia, may also improve 
the quality of the circulation. 

In chronic cases other mechanical impediments to the circulation 
are frequently observed. Partial or complete obliteration of the 
pleural cavity, and pleuro-pericardial adhesions, resulting in cardiac 
displacements, as has been described elsewhere,’ are effective in 
producing dyspnea, cyanosis, etc. Adhesive pericarditis is very com- 
mon, especially in left-sided lesions. In many cases the tuberculous 
lesion in the lung heals more or less, or remains quiescent for years, 
but the patients remain short-winded, with acrocyanosis, etc., and a 
diagnosis of “heart disease’ is made. 

In these cases murmurs are often heard over the region of the cardiac 
apex. Commonly the murmur is systolic in time and may be trans- 
mitted to the axilla. In rare instances I have heard a presystolic 
murmur over the mitral area, but at the necropsy no changes were 
found in the valves to account for it. It is these cases that are often 
brought forward as proof that the coexistence of mitral stenosis with 
pulmonary tuberculosis is not unusual. Retraction of the left lung 
which contains a large cavity exposes the heart, and a thrill may be 
felt over the cardiac apex, but even this should not invariably be taken 
as proof that there is an obstruction to the flow of blood through the 
mitral valve. These murmurs are clearly the result of cardiac dis- 
placements and pleuro-pericardial adhesions. 

The effects of pulmonary tuberculosis on the circulatory organs are 
also seen in the terminal stages of the disease when myocarditis of 
toxic origin, and also tuberculous implication of the adrenals, result 
in heart failure, extremely low blood pressure, terminal edema of the 
extremities, edema of the lungs, etc. Some of these patients, appar- 
ently holding their own, die suddenly owing to heart failure. 

Effects of Heart Disease on Pulmonary Tuberculosis.—Many authors 
have stated that congenital hypoplasia of the heart muscle is a pre- 

1 Arch. Int. Med., 1921, 28, 62. 
2 Fishberg: Arch, Int. Med., 1914, 13, 656. 
38 


594 RECIPROCAL RELATIONS 


requisite, or a predisposing factor, for tuberculosis (see p 127). Clini- 
cal, roentgenographic, and autopsy confirmation is not lacking. It 
appears, however, that in the vast majority of cases of early phthisis 
the heart is normal in size, and that only with the progress of the 
tuberculous disease it participates in the wasting process of the organs 
of the body, especially the muscles. In other words, the small heart 
seen in phthisical patients is to be considered an expression of the 
general cachexia of phthisis, a phenomenon observed in other wasting 
diseases, notably cancer. 

Some eighty vears ago Rokitanskv asserted that disease of the heart 
and bloodvessels, producing passive congestion of the lungs, are 
preventive of phthisis. Further clinical observation and autopsy 
records embracing thousands of cases have confirmed the opinion of 
this pioneer pathologist. It appears that individuals suffering from 
mitral stenosis are only rarely affected with active and progressive 
tuberculosis of the lungs. 

This antagonism, as far as we know at present, refers only to tuber- 
culous disease. Infection with tubercle bacilli occurs in cardiacs 
practically as frequently as in others. But, owing to the congestion 
and plethora of the lesser circulation produced by the stenotic cardiac 
valves, active tuberculosis is prevented. On the other hand, in con- 
genital heart disease, pulmonary stenosis, tuberculosis is the cause of 
death in nearly all who have survived the first decenium. Here the 
condition is just the opposite of that in mitral stenosis. ‘The blood 
pressure in the pulmonary artery and lungs is low, and there is a distinct 
anemia of the lung tissues. 

Persons suffering from disease of the aortic valve at times develop 
pulmonary tuberculosis, but the lung lesion, as a rule, pursues a very 
benign course. ‘This observation has been made by the writer repeat- 
edly; no acutely progressive case of phthisis has been seen in a patient 
with aortic valve disease, especially when this is accompanied by 
aortitis. Perhaps the most plausible reason that can be assigned is 
that aortic disease is often due to tertiary syphilis, or atherosclerosis, 
both of which are accompanied by sclerotic changes in various visceral 
organs, including the lungs. On the other hand, in cases of aneurism 
of the aorta tuberculous lesions at times develop in the area of lung 
tissue contiguous to the blood tumor. Here we deal with tuberculosis 
favored by compression of the pulmonary parenchyma, which is at 
times also observed in intrathoracic malignant neoplasms. They are 
of little interest clinically, though the pathologist may find suggestive 
hints for further study of these cases. 

Infectious Diseases. The Exanthemata.— Among the acute endemic 
diseases of childhood, scarlet fever is only rarely followed by tuber- 
culosis, and some writers have maintained that there is a distinct 
antagonism between these two maladies (Rilliet and Barthez). The 
acute sequels of scarlet fever are mainly suppurating glands, nephritis, 
and arthritis. These, as will be shown later on, are distinctly antago- 


INFECTIOUS DISEASES 595 


nistic to the development of tuberculosis. The writer has not observed 
any reactivation of tracheo-bronchial adenopathy after scarlet fever, 
as is the case with measles. The same is true of osseous and articular 
tuberculous lesions. 

During epidemics of measles very few tuberculous children escape, 
and after the acute exanthema has passed many show symptoms and 
signs of reactivation of the tuberculous process. Intrathoracic glands, 
which may have given no, or only slight, trouble, become actively 
diseased, suppurate and involve neighboring chains; even tuberculous 
lesions in bones and joints have been observed to reactivate after an 
attack of measies. A large proportion of cases of bronchopneumonia 
following measles is tuberculous, and is probably due to rupture of 
suppurating intrathoracic glands and flooding the lungs with tuber- 
culous pus. However, this seems to be mainly the case with children; 
in adults, measles appears to have no such effect. The extensive 
epidemics of measles among our troops during the World War have not 
increased the morbidity and mortality from pulmonary tuberculosis. 
At any rate, there seems to be no evidence to this effect. 

With smallpox we have had no experience, but writers of former 
generations stated that there seemed to exist some antagonism between 
it and tuberculosis. Antivaccination agitators have maintained that 
vaccinia predisposes to the development of phthisis. But the fact 
that the mortality from tuberculosis has declined in all civilized 
countries in which vaccination has been general speaks against this 
view. Some have mentioned the possibility of transmitting tuber- 
culosis by vaccination. But there is no authentic case on record of 
this ever having occurred. 

Whooping Cough.—Latent tuberculosis is often reactivated by 
pertussis and, in children, tuberculous bronchopneumonia is one of 
the most dreaded sequels of this disease. ‘The combination of pertussis 
and tuberculosis in adults has been observed by the writer in several 
instances. In all the tuberculous process was aggravated, and in one 
it seemed as if the whooping cough was responsible for the fatal issue. 

Influenza.—The recent pandemics of influenza have shown that this 
disease hardly has any influence on the origin, course, and termination 
of pulmonary tuberculosis. The fact that during the three years 
following the epidemics the mortality from tuberculosis has declined, 
favors this view. Indeed, the death rates in sanatoriums and hospitals 
for consumptives which were visited by epidemic influenza have not 
shown any rise during the past three years (see p. 128). 

It appears from available evidence, which is quite ample in this 
case, that tuberculous patients are no more liable to suffer from the 
effects of influenza than non-tuberculous. Many writers are under the 
impression that individuals with active tuberculous disease manifest 
a certain degree of immunity against influenza; that proportionately 
fewer are attacked and, when affected, are less likely to fall prey to 
complicating bronchopneumonia than others. ‘The low rates of mor- 


596 RECIPROCAL RELATIONS 


tality and morbidity, during the epidemics, of tuberculous patients 
compared with the administrative staffs of these institutions, has 
raised the question why the weaker stand more chance of survival 
during epidemics of influenza than the healthy and vigorous.! 

The symptoms and course of influenza does not materially differ 
from those observed among others. ~ In but few has an extension of the 
tuberculous process in the lungs been observed. The liability to 
pheumonic complications appeared much less than in previously healthy 
individuals. After four to six days of fever, weakness, in some instances 
hemoptysis, ete., the symptoms abated, and the original disease, 
tuberculosis, pursued its course as if no complication had occurred. 
The fever chart (Fig. 114) is characteristic of this class of cases, which 
were in the majority. As far as physical signs indicated, no changes 
were found in the tuberculous lesions in most cases. 


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In a small minority of cases, irrespective of the stage of the tuber- 
culous disease, though there seems to be evidence to the effect that 
incipient and quiescent cases were more liable to this complication, 
bronchopneumonia developed. In afebrile cases of tuberculosis the 
temperature rose, reaching 103° to 105° F., rarely higher (Fig. 115). 
In the majority of instances the onset was gradual, though in a few it 
was sudden and preceded by a chill. Dyspnea and cyanosis were 
prominent symptoms in most cases, and weakness, at times prostration, 
was pronounced. At this period, the third or fourth day, physical 
signs of bronchopneumonia may be made out over one base, or both— 
diminished breath sounds, moist rales, at times bronchial breathing, 
and dulness. It is noteworthy that only rarely have old tuberculous 
lesions given indications of reactivation; in most cases the physical 
signs of the tuberculous lesion remained unaltered.” 

In most instances the fever kept on for ten days to two weeks; in 
others it lasted for several weeks (Fig. 116). Deferred defervescence 


1 See Fishberg: Am. Rev. of Tubercul., 1919, 3, 532. 
2 See Fishberg and Boas: Am. Jour. Med, Sci., 1920, 160, 214, 


INFECTIOUS DISEASES 597 


was, however, rare. In patients with advanced and progressive tuber- 
culosis the inevitable was simply hastened by the complicating influenza; 
but this was not the rule in our cases. Many far-advanced cases passed 
through uneventfully, and the tuberculous process then pursued its 


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Fie. 115.—Influenzal bronchopneumonia. Temperature curve uninfluenced by 
previous fever. 


course. On the whole, it appears that the outlook for recovery was 
much brighter in moderately advanced than in incipient cases. It was 
surprising that in the majority of cases no after effects were noted. 
In some instances the residual bronchial catarrh remained, but even 
this disappeared in time. In non-tuberculous, influenza leaves, at 
times, signs of localized pathological processes in the bronchi, lungs, 


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and throat, causing chronic cough, expectoration, etc. These are 
often mistaken, and treated for tuberculosis. It is important that they 
should be differentiated. Details about the diagnosis of these lesions 
are given elsewhere (see p. 542). 


598 RECIPROCAL RELATIONS 


Typhoid Fever.—That typhoid fever has not been shown to be a 
predisposing factor to tuberculosis has already been stated (see p. 129). 
Recently the problem of the coexistence of the two diseases has come 
in for discussion because of the problem of reactivation of dormant 
tuberculous lesions by antityphoid inoculation. Formerly several 
French authors, notably Andral, Louis, Forget, Pidoux, ete., con- 
sidered typhoid altogether antagonistic to tuberculosis and that the 
two diseases are mutually exclusive. Vuillemin pointed out the simi- 
larity of onset in many cases, and insisted that this is the reason why 
some consider typhoid a reactivator of latent tuberculosis; he con- 
cluded that, in a general way, they are antagonistic. Recent experience 
with typhoid in tuberculous patients have shown that the superadded 
infection has no serious effect on the tuberculous process, or the 
symptomatology of the disease. It was observed that patients with 
inactive tuberculous lesions may have typhoid fever without any 
detrimental effects on the pulmonary lesion. During epidemics of 
typhoid at the Trudeau, and the West Virginia State Sanatoriums, 
Brown! and his co-workers, and Clovis and Mills,? did not observe any 
aggravations of the pulmonary process. Most patients recovered. 
It is noteworthy in this connection that several authors report cases 
of acute miliary tuberculosis with typhoid bacteremia. But in these 
cases, described by Busse and Bloomfield, it cannot be justly stated 
that the typhoid bacteremia had a deleterious influence on the tuber- 
culous process which was acute, and would have proved fatal without 
the superadded typhoid infection. 

Syphilis.—Tuberculosis and syphilis being very widespread and 
lasting for many years in the affected patients, it is to be expected that 
the two diseases should often be found in the same person. Some 
authors, especially in France, have maintained that syphilis reduces 
the natural resistance against tuberculosis, and is thus one of the 
most important predisposing factors in phthisiogenesis. On the other 
hand, beginning with Hunter, many have maintained that there exists 
a certain antagonism between these two diseases. 

Syphilis in the Tuberculous.—The association may be encountered 
in two forms: A tuberculous patient acquires syphilis; or one with 
old, tertiary syphilitic manifestations, begins to show symptoms of 
active pulmonary tuberculosis. Empirically we have learned that in 
the former case the outlook is not very bright, though not necessarily 
hopeless, in most cases. The patient, already troubled with symptoms 
of phthisis, loses courage and as soon as the diagnosis of chancre is 
made, he becomes more or less despondent. If the lung lesion is very 
active, especially if it has been running an acute and progressive course, 
antisyphilitic treatment often aggravates the outlook, and the prog- 
nosis is grave. In fact in several cases the writer was convinced that 
the patients perished as a result of the combination of the two diseases. 


1 Am. Rev. Tubercul., 1919, 717. 
2 Jour. Am. Med. Assn., 1920, 74, 297. 


INFECTIOUS DISEASES 599 


It must also be mentioned that in cases in which the lesions of both 
diseases—the tuberculous lung lesion, and the secondary manifestations 
\ are active and manifest tendencies to progression, treat- 
ment is beset with painful obstacles. This is especially true of the 
specific treatment of syphilis. Bothmercury and arsphenamine at times 
aggravate the acute lung lesion, and may induce copious pulmonary 
hemorrhages. 

In intensely chronic tuberculous cases, and in those in whom the 
disease is rather quiescent, things are different. In them, anti- 
syphilitic treatment may be administered with benefit. However, 
even here the lung lesion must be watched for reactions when arsphen- 
amine, mercury, and potassium iodide are administered. At the least 
rise of the temperature, or attack of hemoptysis, the specific treat- 
ment is to be discontinued, or restrained. 

Tuberculosis in Patients with Tertiary Syphilis. —The contrary appears 
to be true of patients with old syphilitic lesions who develop symptoms 
of pulmonary tuberculosis. In them the prognosis of the tuberculous 
lesions is, as a rule, more favorable than in others. Many writers 
speak of an antagonism between syphilis and tuberculosis; at any rate, 
it has not been proved that syphilitic subjects are more apt to dev elop 
phthisis than others. On this point there seems to be an agreement 
among recent authors, such as S. West, Perey Kidd, D’Arcy Power, 
Sir Dyce Duckworth, and many others. This point is well sum- 
marized by Jonathan Hutchinson,' who takes the broad view of the 
subject and concludes that “a tendency to tuberculosis may be modified 
by the introduction of syphilitic poison, not that the latter poison may 
predispose to, or encourage the development of tuberculosis.” 

The cardinal pathological changes in tertiary syphilis are fibrosis of 
the various visceral organs and bloodvessels, and fibrosis is Nature’s 
mode of curing tuberculosis. ‘Though it appears that the lung is one 
of the few organs in the body which escape the action of the syphilitic 
virus very often, still, when tuberculous lesions do occur in old syphili- 
tics, they are very often fibrous in character. Several French authors, 
notably Sergent,” insist that in all cases of fibroid phthisis a careful 
search should be made for stigmata of tertiary syphilis. He maintains 
that inequality of the pupiles absent or sluggish reaction of the pupils 
to light, and particularly leukoplakia of the buccal mucous membrane, 
etc., are very frequently found in cases of fibroid phthisis, and also in 
others in whom old and chronic bronchitis, pulmonary emphysema, 
etc., are diagnosed. 

My personal experience has not been in agreement with that of 
Sergent; a positive Wassermann reaction had only rarely been obtained 
among the numerous cases of fibroid phthisis in the Montefiore Hospi- 
tal, indicating that the vast majority of cases of fibroid phthisis have 
no syphilitic substratum. However, most cases of pulmonary tuber- 





1 D’Arcy Power’s System of Syphilis, London, 1912, 2, 12, 
2 Etudes cliniques sur la tuberculose, Paris, 1919, p. 247. 


600 RECIPROCAL RELATIONS 


culosis in patients with tertiary syphilis have been found to run a 
benign and sluggish course: The patients cough, expectorate, have 
pulmonary hemorrhages for many years, but are, as a rule, afebrile. 
The most annoying symptom appears to be dyspnea, which is only 
rarely lacking. It is noteworthy that emaciation is not a common 
symptom; the majority of the patients are more or less obese. Because 
demonstrable tubercle bacilli are rare in the sputum, many of these 
patients are treated for years for bronchitis, asthma, pulmonary 
emphysema, etc. In many instances there are syphilitic lesions which 
skilful and experienced laryngologists find difficult to differentiate 
from tuberculous laryngitis and only the therapeutic test clears up. 
But even the pulmonary lesion is not easily diagnosed. The “hybridity 
of the lesions,” as Sergent refers to them, is often perplexing to the 
clinician. The results of the Wassermann test are not always decisive 
for obvious reasons. One of the most important features of these 
cases is the high blood-pressure. In all cases of tuberculosis with 
vascular hypertension, a reason should be sought, and it will be found 
that, in addition to the specific lung lesion, there is either a cardiac, 
renal or gouty substratum, or, more commonly, tertiary syphilis. 

The most important feature of the association of pulmonary tuber- 
culosis with tertiary syphilis is that the prognosis is very good, and 
that antisyphilitic treatment, arsphenamine, mercury, and the iodides, 
render excellent therapeutic service in relieving the symptoms of both 
diseases. It is probably for this reason that many writers, in this 
country B. L. Wright, have reported success with mercury in the treat- 
ment of pulmonary tuberculosis. Morerecently arsphenamine has been 
urged in some cases. A French author, G. Milian,! speaks of hetero- 
therapy, the treatment of a disease with the specific medication for 
another disease, in this connection. 

It is curious that several writers, having observed the good prog- 
nosis of tuberculosis in syphilitic subjects, have suggested that inocu- 
lation with the syphilitic virus might be advisable for therapeutic 
purposes.2. This is mentioned merely as another aspect of the many 
curious “cures” that have been suggested for tuberculosis. 

Mixed Infection.—Soon after the discovery of the tubercle bacillus 
many authors, finding pyogenic microédrganisms in the secretions and 
excretions of tuberculous patients, maintained that most of the symp- 
toms of phthisis are due to mixed infections. Especially the fever, 
nightsweats, amyloid changes in the visceral organs, etc., were attrib- 
uted to superinfection with streptococci, staphylococci, pneumococci, 
ete., which are found in the sputum, the contents of cavities, as well 
as their walls, which are often covered with pyogenic membranes. 
This view, held by Cornet, Petruschky, Maragliano, and many others, 
is well expressed by Victor C. Vaughan: ‘“Unaided, the tubercle 


1 Paris Médicale, 1920, 10, 337. 


2 See G. Z. Petresco: Tuberculose et Syphilis, 1903; Quoted from Ztschr. f. Tuberkulose, 
1904, 6, 468. ; 


MIXED INFECTION 601 


bacillus seldom kills, but the microbic tissues caused by its growth 
form a suitable medium for the lodgment and growth of other bacteria, 
and tuberculosis usually terminates as the result of infection. So long 
as the infection is unmixed, the progress of the disease is slow.” That 
this view is not exactly in agreement with known facts is seen in acute 
general miliary tuberculosis, which is invariably fatal, and it is here 
that only the specific germ is found. On the other hand, many 
advanced cases of phthisis, with large cavities, the sputum containing 
large numbers of pyogenic microdrganisms in addition to the tubercle 
bacilli, have no fever, anorexia, nightsweats, emaciation, etc. 

The term mixed infection has not always been properly applied by 
many authors. Secondary, or superimposed, but transient infections, 
occurring during the course of phthisis, such as influenza, pneumonia, 
etc., are no more mixed infections than is diphtheria, gonorrhea, or 
malaria. A patient suffers from mixed infection when, in addition to 
the tubercle bacilli, other pathogenic microérganisms have entered the 
tissues of the body and are influencing the course of the disease per- 
manently, or for a long time. Some authors, in this country Roswell 
T. Pettit,! have maintained that this is often the case in phthisis. 
Pettit isolated pneumococci and streptococci from the blood of more 
than one-third of cases of tuberculosis, and he concludes that “ not only 
are true secondary invading organisms of frequent occurrence in pul- 
monary tuberculosis, but further, that in many instances these organ- 
isms, entering the blood stream, constitute a complication of extensive 
pathological significance.” 

Other authors, with a view of proving the importance of mixed 
infections with pyogenic microdrganisms, have pointed to the blood 
count in this disease. But we have shown that a real leukocytosis 
is rare in phthisis, and particularly in the acute miliary form of the 
disease (see p. 444). The increase in the number of white blood cells 
to 12,000 or 15,000 does not constitute leukocytosis due to septic 
infection. 

It must be emphasized in this connection that when pyogenic 
microorganisms are found the sputum, or in the contents of cavities, 
it does not necessarily prove that they are responsible for the symptoms. 
In the first place, they may not have come from the lungs but alto- 
gether from the upper respiratory passages and the mouth. ‘To be 
sure, various methods have been devised to wash the sputum which 
has been carefully collected, but according to painstaking bacterio- 
logists they have proved unsatisfactory. Radcliffe,’ in fact arrives at 
the conclusion that ‘when a true secondary infection is present, it is 
impossible to remove the causative microbe from the sputum by 
washing, just as it is impossible to remove the tubercle bacillus.” 

The weight of current opinion is against the contention that the 
symptoms of tuberculosis are in a great measure due to superimposed 


1 Jour. Infect. Dis., 1911, 9, 237. 
2 Ztschr. f. Tuberkul., 1913, 21, 258. 


602 RECIPROCAL RELATIONS 


infections. To be sure, in more than 50 per cent of cases of chronic 
phthisis pyogenic germs are found in the sputum, and also in the walls 
of pulmonary cavities. But it appears that they exist merely as 
saprophytes. Some authors have, in fact, referred to this form of 
superinfection as passive mixed infection, giving no symptoms. At 
any rate, clinically it cannot be identified, because the symptoms 
caused by the tubercle bacilli cannot be differentiated from those 
produced by the superadded microbic invasion. Acute exacerbations 
during the course of phthisis are, at times, undoubtedly due to these 
mixed infections, but the hectic fever, which bears great similarity to 
pyogenic septic fever, amyloidosis, etc., have been proved to be due to 
the tubercle bacilli, and the absorption of toxins from the decayed 
tuberculous tissues in the lungs. 

A non-tuberculous bacteremia is extremely rare in phthisis. Investi- 
gations by Sorgo,! Radcliffe, Reiche,? Jochmann,’ Brauer and Peters,’ 
and many others, have shown that the blood is sterile in nearly all 
cases of chronic and progressive tuberculosis, excepting, of course, that 
in some cases tubercle bacilli are found (see p. 284). Streptococci and 
staphylococci may be found in very rare instances in the blood of 
tuberculous patients, but this is usually a terminal phenomenon, 
occurring a few days before death when the defensive forces of the 
body have been paralyzed. 

Constitutional Diseases.— The group of diseases classed as “ consti- 
tutional” offers some very good examples of the effects of other patho- 
logical processes on the origin and course of pulmonary tuberculosis. 
Among these the most important are those manifesting themselves as 
chronic rheumatism, gout, migraine, neuralgia, myalgia, obesity, 
asthma, stone in the kidney and gall-bladder, premature athero- 
sclerosis, diabetes, etc. In short, the group called by the French 
“arthritism’” and in English and American literature ‘“lithemia,”’ 
or the arthritic diathesis. It appears that, with the exception of 
diabetes, persons afflicted with any of these diseases are comparatively 
immune to progressive pulmonary tuberculosis. When tuberculosis 
does occur, it runs a mild, benign and sluggish course. 

This was already noted by Morton, who, in his Phthisiologia, pub- 
lished in 1689, said “arthritic phthisis is an asthmatic form of the 
disease, noteworthy more for the viscosity of the bronchial secretions 
than by its obstinate cough.” 

Rheumatism.—Tuberculous rheumatism was first described by 
Chamorro in 1888, Grocco in 1892, and finally by Poncet® in 1897. 
According to these authors tubercle bacilli or their toxins, are frequently 


1 Wien. klin Wehnschr., 1904, 17, 725; Ztschr. f. klin. Med., 1907, 61, 250. 

2 Med. Klin., 1909, 5, 1962. 

3 Deutsch. Arch. f. klin. Med., 1905, 83, 558; Lehrbuch d. Infektionskrankheiten, 
Berlin, 1914, p. 154. 

4 Handb. d. Tuberkulose, 1919, 3, 148. 

5 The literature on this subject may be gleaned from Poncet and Leriche’s Le Rheuma- 
tisme tuberculeux, Paris, 1909. 


CONSTITUTIONAL DISEASES 603 


the cause of acute and chronic mono- and polyarthritis, and various 
arthralgias, at times running a febrile course indistinguishable from 
acute articular rheumatism and subacute and chronic pains in the 
joints, including the spinal column which may or may not end in 
ankylosis. In the chronic cases the general condition of the patient 
remains good, and cardiac complications are rare, while the joint 
symptoms are pronounced. Whether the arthritic symptoms in these 
cases are really caused by the tubercle bacillus or its toxin, 1s a disputed 
problem and will not be entered into here. 

One clinical fact is, however, important for those who care for 
tuberculous patients. It appears that patients with rheumatic troubles 
involving one or more joints, presenting any of the clinical syndromes 
of chronic or subacute rheumatism, only rarely suffer from active and 
progressive pulmonary tuberculosis. There are admitted to my 
service at the Montefiore Hospital annually several cases of arthritis 
deformans, chronic rheumatism, spondylitis, etc., with some symptoms 
and signs of localized lesions in the lungs or pleura. But in nearly all 
no symptoms of active pulmonary tuberculosis can be observed. In 
the extremely rare instances in which there are demonstrable tubercle 
bacilli in the sputum, thus showing that the lung changes are undoubt- 
edly tuberculous, the patients are afebrile and usually well nourished, 
indicating that the process in the lung is in abeyance. 

The same is true of gout. Wunderlich found among 108 gouty 
persons that not one presented symptoms of tuberculosis; Cotton 
states that among 1000 tuberculous patients only 6 showed symptoms 
of gout.t. At the Montefiore Hospital experience has taught us that 
wherever we meet a case of gout, or chronic rheumatism admitted to 
the tuberculosis division with a diagnosis of tuberculosis, there are 
either no symptoms of active lung disease to be discovered after a 
careful and prolonged study of the case, or when the lesion is tuber- 
culous, it is of the sclerotic form, hardly giving any symptoms. Well- 
nourished consumptives, the ‘“‘fat consumptives’”? mentioned else- 
where (see p. 606), are mainly found among arthritic subjects, or 
perhaps of arthritic stock, and also among those who were scrofulous 
during early childhood. Some of these patients have hemoptyses, at 
times copious hemorrhages occur, but a fatal issue is extremely rare; 
some even feel better after the bleeding. Pidoux,? Sokolowski,’ 
Lemoine,’ and others pointed out that the arthritics supply the main 
contingent of curable case of phthisis, and those who, despite tuber- 
culosis, reach an advanced age. 

English authors, whose experience with gout has been extensive, 
confirm these observations. J. E. Pollock believes that “gout, like 


1 In Herard’s article on tuberculosis in Herard, Cornil and Hanot’s La Phtisie Pul- 
monaire, Paris, 1888, p. 367, numerous references are made to the literature on this 
subject. 

2 tudes générales et pratique sur la phtisie, Paris, 1873. 

3 Deut. Arch. f. klin. Med., 1890, 47, 558. 

4 Semaine Médicale, 1900, 20, 103. 


604 RECIPROCAL RELATIONS 


rheumatism, when the specific attack of the disease is developed in a 
ease of tubercle, retards the latter.” Sir Dyce Duckworth also 
considers gout, or the gouty diathesis, as antagonistic to phthisis. 
F’. Parkes Weber' suggests that the resistance of gouty person toward 
tuberculosis is partly due to the meat food (butcher’s meat, eggs, and 
all animal protein foods) which most persons with acquired goutiness 
have been accustomed to indulge in freely during most of their lives. 
“Great meat eaters, if not alcoholic, rarely, even in the most unhygienic 
surroundings, become phthisical.’’ Raw? regards the gouty diathesis 
as antagonistic to phthisis, and he found that blood of gouty persons 
is not a suitable medium in which tubercle bacilli will flourish. 

Cholelithiasis and Nephrolithiasis.— Persons with stone in the kidneys 
or gall-bladder only rarely develop active pulmonary tuberculosis. 
An attack of nephritic or biliary colic is only rarely observed in 
sanatoriums and hospitals for tuberculous patients. Among 128 
subjects who came to autopsy from my service at the Montefiore 
Hospital, not one was found with stone in the kidneys, and only 1 
with stone in the gall-bladder. We are at a loss to account for this 
mutual exclusion. The fact that stone is one of the manifestations of 
the arthritic and uric acid diatheses shows that it is in line with the 
rarity of phthisis in rheumatic and gouty subjects. 

Atherosclerosis.— Patients with atherosclerosis, including aged per- 
sons, as well as those whose arteries calcify prematurely, only rarely 
suffer from progressive pulmonary tuberculosis. In some we find that 
the symptoms of tuberculosis are quite marked, especially the cough, 
expectoration and hemoptysis, which is probably more common than 
in tuberculous patients with elastic arteries, but the symptoms of 
toxemia are usually lacking; there is no fever, nightsweats, emaciation, 
etc. The lesion in the lung tends to fibrosis, and is often circum- 
scribed and limited to one lobe. 

When occurring in young persons, the cause of atherosclerosis is 
frequently syphilis, or interstitial nephritis; and both, as was already 
stated, are antagonistic to tuberculosis. Moreover, atherosclerosis 
is a manifestation of age, or even of senility, and tuberculosis in the 
aged usually pursues an intensely chronic course. It is the tendency 
to fibrosis and calcification, characteristic of atherosclerosis, syphilis, 
and senility, combined with a tendency to the deposit of calcium in the 
tissues, that probably retard the progress of the tuberculous lesion. 
Sunilar conditions are observed in interstitial nephritis and alcoholism. 

Diabetes.—The traditional belief that diabetics are more liable to 
develop pulmonary tuberculosis than those with normal sugar metab- 
olism has been somewhat shattered of late. 5S. Solis-Cohen even 
maintains that the number of cases in which tuberculosis supervenes 
upon diabetes is far less proportionately than the number of cases of 
tuberculosis found among persons whose carbohydrate metabolism is 


1 Lancet, 1904, 1, 924. 
2 Tuberkulosis, 1911, 10, 169. 


CONSTITUTIONAL DISEASES 605 


not obviously disturbed, who, at all events, do not manifest glycosuria 
of glycouresis either persistent or’ permanent. In fact, the large 
percentage of diabetics presenting tuberculous lesions when examined 
at autopsy is not at all formidable when we recall that similar, or even 
higher, percentages are found when careful autopsies are made of 
persons who died from any cause. Thus, Montgomery! found that 
out of 355 autopsies collected from the literature since 1882, including 
his own 25 cases, 138, or 38.9 per cent revealed tuberculous lesions in 
the lungs, mostly in the acute form. This cannot be considered very 
excessive when it is borne in mind that tuberculous lesions are found in 
similar, or even higher, proportions among persons between twenty-five 
and fifty years of age. Joslin found among 1146 cases observed from 
1894 till 1916 only 3.1 per cent with tuberculous lung lesions, which is 
lower than might be expected had their sugar metabolism remained 
normal. 

Symptoms.—From the large number of diabetics with tuberculous 
lung lesions that have come under the writer’s observation, it appears 
that the symptoms of phthisis do not differ materially from those 
observed in others. Some writers, notably Williamson, Magnus-Levy, 
and others, state that hemoptysis and also nightsweats are rare in 
diabetic consumptives. Most writers emphasize that in many cases 
the lesions are localized in the lower lobes of the lungs, and that tubercle 
bacilli may not be demonstrable in the sputum, all of which leads one to 
suspect that, in diabetics, the diagnosis of tuberculosis is made at times 
without a solid foundation. Personal experience in hospital and 
private practice has shown that there is no basis for the supposition 
that the symptoms and signs of phthisis differ materially in diabetics 
from those with normal sugar metabolism. In some, the course 
is progressive, in others, sluggish, while now and then we meet with 
fibroid phthisis which lasts for years without causing great incon- 
venience to the patient. I have met with cases in which both diseases 
lasted for over fifteen years. On the whole, it appears that tubercu- 
losis is diagnosed in diabetics more often than facts would warrant. 

The effects of tuberculosis on the metabolic disease is also of clinical 
interest. Magnus-Levy,? and other writers, have observed that with 
the appearance of symptoms of phthisis there occurs a decrease in the 
amount of sugar eliminated through the urine—in some patients it 
even disappears. Magnus-Levy says that this is due to the anorexia 
and cachexia characteristic of phthisis. But Naunyn observed that 
patients without these symptoms may show increased sugar tolerance 
with the onset of the tuberculous complication. It appears that only 
in mild cases is the increased sugar tolerance to be observed; in those 
with progressive tendencies, especially with acidosis, the elimination 
of sugar continues, as a rule, unabated. This point is to be borne in 


1 Am. Jour. Med. Sci., 1914, 147, 866. 
2 In Kraus and Brugsch’s Spez. Pathol. u. Therapie, Berlin, 1914, 1, 36, 


606 RECIPROCAL RELATIONS 


mind when judging the effects of any method of treatment of diabetes 
in tuberculous patients. 

Rarity of Glycosuria in the Tuberculosis Patients.—It is noteworthy in 
this connection that while tuberculosis often complicates diabetes, the 
contrary is not true. Whenever the two diseases are associated, 
diabetes almost invariably preceded the tuberculosis. West, Raw, 
Montgomery, and many others, have reported this as their experience. 
In the writer’s practice, dealing with thousands of tuberculous patients 
derived from a class peculiarly liable to diabetes (Jews), only 2 tuber- 
culous patients were observed to develop glycosuria while suffering 
from active tuberculosis. Among 31,834 cases of tuberculosis, collected 
from 25 sanatoriums and hospitals in various parts of this country, 
there were 101 (about one-third of 1 per cent) cases of glycosuria and 51 
(about one-sixth of 1 per cent) of diabetes, according to Landis, Funk 
and Montgomery.! Even conceding that some of the cases were 
undoubted diabetics, the percentage is exceedingly low. More than 
1 per cent of the general population in this country is diabetic. Among 
1047 autopsies made on tuberculous subjects only 6 were diabetics, 
and some of these may have been sick with diabetes before the develop- 
ment of the tuberculous lung lesion. In fact, among 373 tuberculous 
cases autopsied in the United States Army, not a single case of diabetes 
was discovered. 

It is not clear why tuberculous patients never become diabetic. 
The fact that diabetes is a disease of excess in food and drink, while 
tuberculosis is one of undernutrition, may be suggestive, but it does not 
explain. 

Prognosis.—In a large proportion of cases the tuberculous disease in 
diabetics runs a progressive course, leading to a fatal termination, 
which could be expected a priori considering that both are wasting 
diseases. But I have seen many in whom the tuberculous process was 
quiescent, or sluggish in its course, lasting for many years. Improve- 
ment may be seen in either, or both, diseases. It also seems that when 
the diabetes is of a severe character the tuberculous process is likely to 
pursue a progressive course, and vice versa. Next to acidosis, tuber- 
culosis appears to be the commonest cause of death in diabetes. Social 
conditions have a great influence; among the well-to-do the association 
of the two diseases is not always rapidly fatal. Having seen healed 
tuberculous lesions in the lungs of individuals who succumbed to 
diabetes, the writer is inclined to the opinion that, while serious, the 
complication is not invariably fatal. 

Obesity.—Pulmonary tuberculosis occurs very frequently in well- 
nourished individuals, but only rarely in the obese in the full sense of 
the word. ‘The reasons are obvious: ‘Tuberculosis, consumption, is 
the direct antithesis of obesity. But now and then we meet with a 
case of undoubted active phthisis in an obese person. As a rule, the 


1 Am. Rev. of Tubere., 1919, 2, 690. 


DYSFUNCTION OF THE ENDOCRINE GLANDS 607 


tuberculous process tends to cicatrization in these fat patients. In 
some instances the pathological process in the lung proceeds from 
infiltration to softening and the formation of large cavities; but the 
excavations are, as a rule, circumscribed and surrounded by dense 
fibrous capsules. The patient keeps on coughing for many years, and 
expectorates sputum containing tubercle bacilli. But hardly any 
symptoms of tuberculous toxemia are observed, excepting perhaps 
dyspnea and cyanosis. 

The prognosis in these cases of “fat consumption” is good, so long 
as there is no fever. But finally, if not carried off by some intercurrent 
disease, fever develops, emaciation becomes pronounced, and the 
patient succumbs with the usual terminal symptoms of phthisis. While 
this occurs in many cases, still it is a rare phenomenon. Fat consump- 
tives live very long; some as long as might have been expected had they 
not developed tuberculous lesions in the lungs. 

At times we observe patients who had always been of average, or 
below the average weight, develop tuberculosis; the lesion in the lungs 
heals by cicatrization and cavity formation, and then they become more 
or less obese. ‘This is commonly seen in women over forty years of age, 
though rarely it occurs in younger persons, of either sex. The obesity 
in these cases is of the plethoric type, and they are liable to more or 
less copious pulmonary hemorrhages which usually give them relief 
for some time. Most of them have mild fever, as many obese persons 
do; they cough and expectorate, etc. Especially annoying is the 
dyspnea, due to both the obesity and the limitation of the breathing 
area in the lungs. 

It appears that the obesity in consumptives is, In many instances, 
due to some dysfunction of the internal secretory glands, as is attested 
by the fact that it occurs frequently in women during the menopause, 
and in men with gonadal tuberculosis (see p. 610). But we also see it in 
patients who have been thoroughly hospitalized; who have spent years 
in various sanatoriums and acquired a knowledge of the great benefits 
to be derived from perfect rest, nourishing food, ete. 

Dysfunctions of the Endocrine Glands.—The association of certain 
endocrine disturbances with pulmonary tuberculosis is quite frequently 
observed. Considering the great prevalence of tuberculosis, it may be 
assumed that in many cases the association is altogether coincidental. 
But in many instances it appears that one disease is either stimulated, 
or arrested in its progress, by the other. This is especially the case 
with dysfunctions of the thyroid, adrenals and the gonads. 

Thyroid Dysfunction.—It is well known that quite a large proportion 
of tuberculous patients present symptoms of hyperthyroidism such 
as more or less bulging eves, tachycardia, a slight tremor, hot flushes, 
sweating, dermographism, and even enlargement of the thyroid gland 
(see p. 290). This cannot be attributed to tuberculosis of the thyroid 
because it has been shown that this gland is relatively immune to the 
tubercle bacillus. Rokitansky never observed a case, and Virchow 


608 RECIPROCAL RELATIONS 


said that no organ is so little disposed to tuberculosis as is the thyroid. 
To be sure, cases have been reported in which the thyroid showed 
tuberculous changes at the autopsy, or after surgical removal; in this 
country Mosiman! reported such cases. But, at all events, they are 
rare. Albert Kocher,? whose experience has been extensive, says that 
the thyroid displays a strong resistance against the virus of tuber- 
culosis, and that tuberculous changes in the gland are observed only 
in extremely rare instances. When the thyroid, derived from tuber- 
culous cases, is examined histologically the changes are those of 
sclerosis, as a rule, the direct antithesis of those found in Graves’s 
disease. Kehl says that he could not find any tuberculous changes in 
the thyroid of 50 tuberculous patients. 

It is not generally appreciated, but it is a fact, that in patients with 
symptoms of hyperthyroidism, tuberculosis, when it does occur, runs 
a very mild course; in many the abortive type of the disease is to be 
seen. In cases in which the differential diagnosis between hyper- 
thyroidism and pulmonary tuberculosis has to be made, we are often 
actually dealing with the coexistence of the two diseases, but the lung 
lesion is so mild, the patient recovering, and remaining with the thyroid 
dysfunction, that we are apt to conclude that the suspicion of tuber- 
culosis was not justified. In progressive cases of phthisis we may note 
symptoms of hyperthyroidism in the incipient stage, but with the 
advance of the tuberculous disease, they disappear. They may also 
disappear when the lung lesion improves, or when the patient is cured 
of his tuberculosis. 

The transitory character of the hyperthyroid symptoms, disappear- 
ing with aggravation, as well as with improvement, in the tuberculous 
process, is rather suggestive. It appears that the tuberculous toxin 
stimulates the thyroid at first, but when the stimulation keeps on for a 
considerable time, it is effective in producing sclerosis of the gland, 
and for this reason we find sclerosis of the thyroid in many fatal cases 
of tuberculosis. Moreover, hyperthyroidism is often found in youthful 
tuberculous patients, in adolescents, in young girls in whom menstrual 
disturbances, dysmenorrhea, amenorrhea, etc., are clinical features of 
the case. 

The mildness of tuberculosis in hyperthyroid individuals was 
observed fifty years ago by Hamburger,’ and Morin‘ noted long ago 
that in tuberculous families the members who have large thyroids 
escape, and when infected, recover. S. Solis-Cohen stated as far back 
as 1887 that a large thyroid is characteristic of immune members of 
tuberculous families. Greenfield® could not find tuberculous lesions 
in any of the fatal cases of Graves’s disease that came under his observa- 


Surg., Gynee. and Obst., 1917, 24, 680. 

In Kraus and Brugsch’s Spez. Pathol. u. Therapie, Berlin, 1919, 1, 819, 989, 
Quoted from Muralt, Med. Klinik, 1913, 9, 1814. 

Rev. Méd. de la Suisse Romande, 1895, 15, 241. 

Lancet, 1893, 2, 1554, 


ao hm Oo te 


DYSFUNCTION OF THE ENDOCRINE GLANDS 609 


tion. Similar experiences have been reported by Bialokour,! Bran- 
denstein,? and others. Among 45 cases of hyperthyroidism observed 
by Saathoff all had signs of tuberculosis, but of a mild type, only 2 
were of the “open” type. Turban,‘ Gerald Webb,® and many others 
have had the same experience. In Webb’s® opinion “the increase 
in the size and function of the thyroid is a phase in the marshalling of 
the body’s defensive forces against the invading disease.’”’ Webb 
quotes Plummer, of the Mayo Clinic, where large numbers of cases of 
exophthalmic goiter are treated, to the effect that tuberculosis is much 
more rare in persons with this disease than in others. 

This is in agreement with our observations presented while discussing 
the status lymphaticus (see p. 588). It is well known that during 
adolescence some youths with symptoms and signs of the lymphatic 
diathesis grow rather fast in height, their hands and feet enlarge, thus 
presenting the stigmata of either dyspituitarism, or dysthyroidism 
(see p.575). Itis just at this period of life that pulmonary tuberculosis 
develops in many persons. It is noteworthy that “doubtful” cases are 
most frequent among adolescents, and that many of these “suspects” 
recover, to tell in later life the usual story that during their early life 
some doctor diagnosed tuberculosis in them. Fr. Kraus’ and Julius 
Bauer® have pointed out that these individuals are liable to develop 
extra-pulmonary tuberculous lesions, but I cannot say from personal 
experience that such is the case. 

Hypothyroid individuals, on the other hand, very frequently suffer 
from active and progressive tuberculosis of the lungs. In fact, in 
thyroid families some children are myxedematous, or cretins, while 
others are tuberculous. W.S. Greenfield speaks of “the great tendency 
in myxedema to tuberculosis. Of course, it may occur in Graves’s 
disease, but as far as I can judge there is no special tendency to 
it. In myxedema it is especially frequent.” In 5 out of 7 fatal 
cases of myxedema, tuberculosis of the lungs was found at autopsy; 
while in none of the cases of Graves’s disease was tuberculosis found 
at autopsy. Greenfield suggests that perhaps thyroid medication may 
be helpful in these cases. Symptoms and signs of hypothyroidism 
are very often noted in far-advanced cases of tuberculosis. 

Dysfunction of the Adrenals.—In a very large proportion of cases 
of pulmonary tuberculosis there are to be seen symptoms pointing to 
dysfunction of the adrenals. The low blood-pressure, as well as the 
weakness and lack of enduring powers, pigmentation of the skin, etc., 
have been attributed to hypofunction of the adrenals. The great 
frequency with which these glands are found affected by tuberculosis 


1 Ztschr. f. Tuberkulose, 1910, 16, 230. 

2 Berl. klin. Wehnschr., 1912, 49, 1840. 

3 Miinchen. med. Wehnschr., 1913, 60, 230. 

4 Beitr. z. Kentniss der Lungentuberkulose, 1899. 

Jour. Labor. and Clin. Med., 1916, 1, 414, 5 Am. Rev. Tuberc., 1921, 5, 266. 
Ztschr. f. Tuberkulose, 1913, 19, 417. 

Konstitutionelle Disposition zu inneren Krankheiten, Berlin, 1917, p. 361. 


39 


ota 


610 RECIPROCAL RELATIONS 


in cases of phthisis, favors the view that they are due to insufficiency 
of the adrenals. Many writers have seen a correlation between the 
excessive function of the thyroid in incipient tuberculosis and the 
insufficiency of the adrenals. On the other hand, Gerald Webb and 
his co-workers found hypertrophy and hyperfunction of the adrenals 
in experimental tuberculosis. 

It is noteworthy that while in nearly 90 per cent of cases of Addison’s 
disease tuberculous changes are found in the adrenals, active tuber- 
culosis of the lungs is very rare in this disease. Most of the lung lesions 
found at the autopsy are of the sclerotic type. According to some 
authors, notably Kxraus, Bauer, Bartel, and others, Addison’s disease 
occurs mainly in individuals of the lymphatic constitution, and the 
lungs are thus shielded against tuberculous changes by the extra- 
thoracic lesions, as we have already shown (see p. 584). In fact, 
tuberculous lesions in the lungs found in many cases of Addison’s 
disease are almost invariably of slight extent and healed. 

The Gonads.— We have already spoken of the rarity of active and 
progressive tuberculosis of the lungs in cases of tuberculosis of the male 
generative organs (see p. 587). In women also it appears that when 
tuberculosis occurs during the menopause, it is apt to run a sluggish 
course, frequently of the fibroid type. In several cases of tuberculosis 
of the female generative organs, verified by examination of the organs 
removed surgically, the lungs have been found free from active disease. 
I have also observed that in such cases, after successful operative 
removal of the tuberculous adnexa, active and progressive tuberculous 
disease of the lungs is likely to be of its appearance. Here again we 
find evidence that extrathoracic tuberculosis is to a certain degree 
antagonistic to pulmonary tuberculosis. 

Many cases of tuberculosis in women over forty years of age show 
the effects of hypofunction of the gonadal organs more than those of the 
tuberculous toxemia. The lung lesion, as has just been stated, is likely 
to be sclerotic and give very ‘little trouble. But symptoms due to 
hypofunction of the ovaries are pronounced. It is difficult to say 
whether the hyperfunction of the thyroid, characteristic of the meno- 
pause, is responsible, but it is a fact that these patients get along for 
many years though showing signs of active tuberculosis. The consti- 
tutional symptoms are very frequently relieved by the administration 
of organotherapeutic products, as will be shown later on. 

The fact that fibroid phthisis is most common in persons over forty 
years of age, and that tuberculosis in the aged pursues, as a rule, a very 
sluggish course, are suggestive in this connection. 

In contrast with the chronicity of phthisis in individuals in whom the 
function of the sex glands is below par, we observe that when the disease 
occurs in youthful individuals, especially at the age of puberty, when the 
function of the gonads is at its highest, the process is very often acute 
and progressive. In boys between sixteen and twenty-five years of 
age, acute pneumonic phthisis is very frequent, and when the disease 


DYSFUNCTION OF THE ENDOCRINE GLANDS 611 


is of the chronic type, it very often shows tendencies to progression; 
soon after the onset we often find that an entire pulmonary lobe is 
involved. Remissions are short-lived. The general appearance of 
these patients is striking to the observant clinician because of the 
pathognomonic “ facies’’ (see p. 299), the ghastly pallor which is quite 
common, and by the high fever and prostration. Arrest of the disease 
may occur, but not as often as in persons over twenty-five years of 
age. Such acute cases are rare among persons over thirty, and 
exceptional over forty-five, excepting, of course, miliary tuberculosis, 
which is the last straw in many cases of chronic pulmonary phthisis. 
One of the characteristics of phthisis at the age of puberty is the 
uncommonly high stature (see p. 576), which again points to hyper- 
function of the gonads. 

The relationship of phthisis to puberty is, however, best seen in 
girls. When fully developed, phthisis often results in amenorrhea. 
But it has been observed, first by H. Hanford,! that early or excessive 
menstruation in young girls is often associated with tuberculosis. He 
stated also that the female children of phthisical parents tend to 
menstruate unduly early, and excessive. More recently Scherer,’ in a 
study of 10,216 cases of tuberculosis in women arrived at somewhat 
similar conclusions. He found that in girls who menstruate early, or 
excessively, the prognosis of tuberculosis is more grave than in those 
who begin to menstruate later and have either a normal or scanty flow. 
This may perhaps be correlated with the observation of botanists 
that sickly and weakly plants blossom earlier and bear more fruit, 
numerically, than healthy and vigorous ones. We have already referred 
to the fertility of tuberculous individuals (see pp. 298 and 579). 

More recently this has been confirmed experimentally by Hans 
Mautner.*? He found that when castrated guinea-pigs are infected 
with tubercle bacilli they live longer than normal controls, while thy- 
roidectomized animals die sooner. He also reports that castrated 
animals, when infected, display strong tendencies to recovery, the 
lesions are localized; while the control animals become emaciated, the 
‘astrated ones showed strong tendencies to the deposition of fat on the 
body. 

It is well known that the establishment of puberty has a more 
profound effect on girls than on boys, and that it occurs earlier in the 
former. And at this period of life, the mortality from tuberculosis 
is higher among females than among males. As can be seen from the 
table on page 85, the rates per 100,000 were among girls ten to fourteen 
years of age, 29.4, and among boys, only 12.2; between fifteen and 
nineteen years of age, girls, 110.9, and boys, 79.6. After twenty- 
five years of age, the mortality is higher in men than in women. 
Vital statistics in other countries are to the same effect (see Figs. 10 
and 11). 

British Med. Journal, 1887, 1, 153. 


1 
2 Beitr. z. Klinik. d. Tuberkul., 1921, 40, 7. 
3 Monatsschrift f. Kinderheilk., 1921, 21, 38. 


612 RECIPROCAL RELATIONS 


Gastro-intestinal Diseases.—The reciprocal relations between 
diseases of the gastro-intestinal tract and pulmonary tuberculosis 
have been discussed in Chapter XI. While ancient authors spoke 
of “gastric phthisis,” it may be stated that we do not know of any 
disease of the stomach which predisposes to pulmonary tuberculosis, 
or is found in phthisical patients with sufficient constancy to make it 
pathognomonic of the disease. The anorexia of phthisis is easily 
explained by the fever, cough, expectoration, ete.; while the emetic 
cough, so often troubling phthisical patients, is not due to any struc- 
tural or functional changes in that viscus. Gastric ulcer is at times 
found in patients suffering from tuberculosis, but not more frequently 
than in non-tuberculous. In 128 autopsies from my service at the 
Montefiore Hospital only 1 was found with an ulcer, and it was not 
of a tuberculous nature. 

Intestinal ulcerations occur very frequently in tuberculous patients 
(see p. 554) but they are due to the same cause as the lung disease. 
There are, however, two intestinal diseases in which there have been 
observed certain relations to pulmonary tuberculosis; they are appen- 
dicitis and fistula-in-ano. 

Appendicitis. —In many tuberculous patients with acute or subacute, 
or adhesive pleurisy of the membrane covering the lower lobe of the 
right lung, symptoms and signs not unlike those of appendicitis are 
often found. This is also true of ulcerations in and near the cecum, 
or the peritoneum covering that part of the bowel. It is for this 
reason that many authors have reported that a large proportion of 
tuberculous patients suffer from appendicitis requiring surgical inter- 
vention, while others have maintained that the contrary is true. 

The number of patients with long-standing pulmonary tuberculosis 
who have abdominal scars indicating operations for appendicitis is 
high; for this reason also some authors have stated that appendicitis 
is an etiological factor in tuberculosis. Faisans, Walther, Siredey, 
Claisse, Thiroloix, and especially Sergent,! are of this view. Sergent 
believes that excessive meat eating, in which tuberculous patients 
often indulge is responsible. He suspects every patient with chronic 
appendicitis of tuberculosis. Letulle found that 30 per cent of con- 
sumptives present inflammatory lesions of the appendix, and Bialokur? 
maintains that from 25 to 30 per cent of all phthisical patients suffer 
from chronic appendicitis, and 50 per cent show tuberculous lesions 
of this rudimentary structure. 

The clinician will become suspicious when he finds that most patients 
with symptoms of appendicitis show signs of pleurisy in the right side 
of the chest, especially the pleura covering the lower lobe is found 
inflamed or adherent. The referred pain in such cases have already 
been described in detail (see p. 483). It appears that those who care- 
fully examine the chest for signs of pleurisy have very few tuberculous 


1 fitudes cliniques sur la tuberculose, Paris, 1919, p. 368. 
2 Internat. Zentralblatt. f. ges. Tuberkuloseforschung, 1915, 9, 137, 


CIRRHOSIS OF THE LIVER 613 


patients who need operations for appendicitis. Gerald Webb! is of 
this view. At the Montefiore Hospital we only rarely see a case of 
appendicitis requiring surgical intervention among the tuberculous 
patients. The pain in the right iliac fossa often seen in tuberculous 
patients may also be due to tuberculous ulcerations of the cecum, 
or localized peritonitis in that region, and more commonly to diaphrag- 
matic pleurisy. 

Fistula-in-Ano.—The association of fistula-in-ano with tuberculosis 
has been noted for generations, and some have maintained that a 
fistula is a sure indication of an active lung lesion. Hartmann stated 
that 5 per cent of tuberculous patients have fistulz, a proportion which 
is rather excessive; less than 2 per cent of patients coming under the 
writer’s care have been found with anal fistule. 

Many surgeons state that the vast majority of fistule are in them- 
selves tuberculous. Among 197 cases reported by Melchior? 61 per 
cent were tuberculous; in Goetz’s’ series the proportion was 43 per cent, 
while other authors found it much less. Harvey B. Stone,‘ in a recent 
study of the question, hazards the estimate that probably in 15 to 30 
per cent of all fistulee cases a fundamental relationship with tubercu- 
losis may be established. The difficulties in establishing the tuber- 
culous nature of fistulz lies in the fact that nearly all, in addition to 
tubercle, have also been infected with pyogenic microdrganisms, and 
the result is that the characteristic microscopic structures are not 
easily discerned; obviously, because of mixed infection, inoculation 
tests are likely to prove misleading. 

It has been the experience of the writer that most tuberculous 
patients with fistula-in-ano do well; the process in the lung is usually 
quiescent or latent, so as to render the diagnosis doubtful. For this 
reason, probably, the diagnosis is not made as frequently as facts would 
warrant. Moreover, it appears that after surgical intervention these 
fistulee recur in a large proportion of cases. As long as the fistula keeps 
on discharging, the pulmonary lesion is likely to remain latent or 
quiescent. But in the comparatively few cases in which operation is 
successful in closing up the fistula, the process in the lung is likely to 
become active and progressive. I have seen numerous cases of this 
sort. Melchior’s statistics bear out this point. For this reason it 
has been my practice recently to discourage operations for fistula-in- 
ano, so long as it is not unbearably troublesome. In most cases 
operated on, or when the fistula closes up, the pulmonary lesion flared 
up within a few months or years. Similar effects of operations on 
other extrathoracic tuberculous lesions have already been mentioned. 

Cirrhosis of the Liver.—Many writers have spoken of a frequent 
association of hepatic cirrhosis with pulmonary tuberculosis. It 


1 Tr. Nat: Tuberc. Assn., 1916, 13, 202. 

2 Beitr. z. Klinik d. Chirurgie, 1910, 70, 475. 
3 Inaug. Diss., Tiibingen, 1916. 

4 Am. Rev. Tuberculosis, 1917, 1, 548. 


614 RECIPROCAL RELATIONS 


appears that many patients suffering from cirrhosis succumb finally 
with symptoms of pulmonary, and at times, peritoneal tuberculosis. 
According to Rolleston,! the cause of death in hepatic cirrhosis is 
pulmonary tuberculosis in 12 to 14 per cent of cases. He compiled 
statistics of 584 cases of cirrhosis obtained by adding together the 
figures in the statistics of Lancereaux, St. George, Kelynack, and Yeld, 
and showed that tuberculous lesions were found in the lungs in 1382, 
or 22.6 per cent: 

In pulmonary tuberculosis the liver is affected very frequently; in 
fact, in a very large proportion of fatal cases miliary tubercles are found 
in the liver; in others, tuberculous abscesses, due to focal necrosis; 
fatty degeneration is seen in the vast majority of fatal cases, and 
amyloid changes in those who, for a long time, suffered from suppura- 
ting and cavitary lesions in the lungs or other organs. Several French 
authors, notably Hanot and Gilbert, have maintained that cirrhosis 
is often found in patients who died from pulmonary tuberculosis, and 
they also brought some experimental evidence to the effect that 
tubercle bacilli may be instrumental in inducing hepatic fibrosis with 
resulting destruction of the parenchymatous cells. However it appears 
that this is exceptional, and even when occurring in far-advanced 
stages of phthisis, it is of little clinical importance, for obvious reasons. 
That it is rare, is seen from Lorentz’s statistics of 4337 autopsies, among 
which 111 were cases of cirrhosis. He found that of those who died 
from cirrhosis, 20 per cent had tuberculous lesions, while those who died 
from tuberculosis showed hepatic cirrhosis in only 2 per cent of cases. 

Cancer.— Ever since Rokitansky, in 1841, observed what he con- 
sidered a distinct antagonism between tubercle and cancer, many 
authors have brought forward evidence in substantiation of this 
contention, while others have denied it. Rokitansky found that 
organs which are liable to cancerous infiltration, as the ovary, the 
salivary glands, the stomach, esophagus, rectum, etc., are only rarely 
affected by tubercle; conversely, organs frequently showing tuber- 
culous changes, as the lungs, the ileum, etc., are only rarely affected 
by malignant neoplasms. 

Autopsies performed on large series of cases seem to substantiate 
Rokitansky’s opinion. Thus, Otto Lubarsch? reported 6536 autopsies, 
among which 2668, or 40.8 per cent, were found tuberculous, and 569, 
or 8.7 per cent, carcinomatous. Of the tuberculous series 117, or 4.4 
per cent, were carcinomatous; while of the 3868 non-tuberculous, 452, 
or 11.7 per cent, were cancerous; of the 569 cancerous, 117, or 20.6 
per cent, were tuberculous, while of the 5967 non-cancerous, 2551, or 
42.7 per cent, were tuberculous. Among 1445 necropsies of persons 
who died from cancer compiled from the literature by Broders,’ only 
236, or 16.3 per cent, showed associated tuberculous lesions, which, 


1 Diseases of the Liver, 1905, pp. 221, 281. 
2 Virchows Archiv, 1888, 111, 280. 
8 Jour. Am. Med. Assn., 1919, 72, 390. 


CANCER 615 


compared with the high percentage found in the general run of autop- 
sles, ranging usually upward of 50 per cent, shows that the two diseases 
are not commonly found in the same individual. Landis' reports 
633 autopsies performed at the Phipps Institute, all tuberculous, and 
among which there was not a single case in which there was associated 
cancerous growth. Roger Williams? found tuberculous lesions only 
twice in 136 cancer autopsies, and he quotes Kelynack, of the Man- 
chester Infirmary, who found it only twice in 145 similar autopsies. 
Likewise, McCaskey* making autopsies on 281 cancer patients found 
tuberculous lesions only in 1.25 per cent; in the non-cancerous its 
frequency was nearly twenty times as great. James Kingston Fowler* 
also states that it is very rare indeed to find tuberculosis and cancer in 
active progress at the same time. 

We do find, however, in many cases of fatal cancer evidences of 
tuberculous lesions in the lungs at the autopsy. These are mainly of 
two varieties: In most cases the tuberculous lung changes are sclerotic, 
or calcified, practically healed; in others, especially in those who died 
from malignant neoplasms of the intrathoracic organs, pressure of the 
tumor on the contiguous parts of the lungs stimulates the reactivation 
of dormant tuberculous. lesions. The writer has seen 2 cases of 
cancer of the lung with old tuberculous cavities, which, however, 
remained inactive while the neoplastic process progressed. In 2 
cases of cancer of the lung, verified by autopsy, tubercle bacilli were 
found in the sputum. 

The reason why there is a certain degree of antagonism between 
tuberculosis and cancer is not known at present with our meager 
knowledge of the etiology of malignant neoplasms. The suggestion 
has been made that the age incidence of the two diseases is responsible, 
tuberculosis occurring mainly before thirty-five, and cancer above 
that age. But this does not hold, because tuberculosis is not at all 
uncommon in persons above forty years of age, and it is in these 
persons, of the cancer age, that tuberculosis only rarely develops once 
they have malignant tumors. 

There is hardly anything of interest about the clinical manifestations 
in the rare cases in which the coexistence of the two diseases is dis- 
covered. At times when a patient with carcinoma of the bronchi or 
lung develops tuberculosis, tubercle bacilli may be found in the sputum, 
and thus some doubt is cast as to the correctness of the diagnosis of 
pulmonary neoplasm, as had occurred in 2 cases under the writer’s 
care. But it appears that the severity of the symptoms of cancer 
obscures the symptoms of tuberculosis, and in due time either metas- 
tasis, or some other feature of the case, clears up the diagnosis. 


1 Quoted from Hoffman, The Mortality from Cancer Throughout the World, Newark, 
1915, p. 188. 

2 Twentieth Century Practice, 1908, 17, 270. 

3 Am. Jour. Med. Sci., 1902, 124, 97. 

4 Diseases of the Lungs, London, 1898, p. 316. 


616 RECIPROCAL RELATIONS 


Insanity. — or generations it has been observed that the tuberculosis 
morbidity and mortality in insane asylums is exceedingly high; in some 
as much as three or four times that of the general population. This 
fact, in connection with the peculiar psychology of the consumptive, 
has led some authors to see a correlation between tuberculosis and 
mental alienation. 

It has been an almost universal observation that mental defectives 
are more liable to develop tuberculosis, and to die as a result of this 
disease, than the average population. This is particularly true of 
inmates of institutions for feeble-minded, in which more than 50 per 
cent of deaths have been due to pulmonary tuberculosis. Among the 
insane about 30 per cent of deaths are due to this cause. Those 
suffering from the depressive psychoses, and dementia precox, are 
most likely to contract phthisis. 

As far as we know it is not insanity per se that is the predisposing 
cause to tuberculosis. When we bear in mind the mental condition 
of the insane, the overcrowding in the institutions, the carelessness of 
the patients as regards food and personal hygiene, it is not surprising 
that many contract the disease in whose etiology these factors play 
such a great role. This is confirmed by the high tuberculosis mortality 
in asylums in backward countries, where the hygienic surroundings, and 
food given the patients, leave much to be desired. In England and 
Wales it was observed that during the World War, when the adminis- 
trative personnel of the asylums was depleted, the mortality from 
tuberculosis showed an appalling increase; among the female patients 
the increase was not as large as among the males, for obvious reasons. 
On the other hand, in this country, while quite high, the tuberculosis 
morbidity and mortality are not as high as observed in European 
institutions. Thus among 962 cases of psychosis coming to autopsy 
in the Manhattan State Hospital for the Insane in New York, active 
pulmonary tuberculous lesions were found only in 131 cases, or 18.60 
per cent (Irving J. Sands). This low incidence may be ascribed partly 
to greater diligence on the part of the pathologists in searching more 
for changes in the nervous system than in the lungs, yet, even so, it is 
much lower than has been observed in other institutions. Perhaps the 
better care and food are responsible. 

The diagnosis of tuberculosis in the insane is rather difficult in many 
cases. A mental defective does not complain of the mild symptoms 
characteristic of incipient tuberculosis, and in institutions the disease 
is discovered mostly when it is far advanced. When diagnosed, it is 
difficult to institute proper treatment in mental defectives because of 
lack of codperation on the part of the patients. 

While tuberculosis is common in the insane, the reverse does not 
hold. Insanity is rare among tuberculous patients. The psychic 
manifestations of the tuberculous, which have already been referred to 
(see p. 294), are mainly of toxic origin, due to the constant absorption 
of toxins ffom the tuberculous lesions. But some authors have seen 


INSANITY 617 


in this a sufficient cause for limiting the legal responsibility of tuber- 
culous patients (Baccelli, Saxe, Jessen, Microli).!- They point to the 
fact that the psychic state of the average consumptive in the advanced 
stages of the disease shows marked divergences from what we are wont 
to consider normal. The oscillating emotional manifestations, the 
alternating moods, changing quickly from supreme exaltation to 
extreme depression, and the lack of appreciation of the true condition 
even during the most ominous periods of the disease, show that the 
mind of the tuberculous patient is not in equilibrium with his withering 
body. Some have drawn a striking analogy between the consumptive 
who is in a state of intoxication by the toxins of the tubercle bacilli 
and decayed pulmonary tissue, and the alcoholic. Indeed, the external 
appearance of the consumptive, walking around in a febrile state, is 
somewhat similar to that of one under the influence of alcoholic intox1- 
cation. The bright eyes, the dilated pupils, the flushed cheeks, 
remind one of alcoholic intoxication, as Microli has pointed out. 
Mentally, also, there are great similarities: The flickering intelligence, 
which brightens up suddenly for a few hours soon to be followed by 
mental depression; the impulsive actions, the perverse stubbornness 
and egotism, all of which, at times, lead to criminal, or antisocial acts, 
combined with the quick transitions from optimism to pessimism, are 
seen among both alcoholic and far-advanced tuberculous patients. 
That these are mainly due to the tuberculous toxemia is shown by the 
fact that injections of tuberculin have been observed to either engender, 
or to accentuate these psychic conditions. 

For these reasons, alienists who are in favor of limiting the legal 
responsibilities of those who are so far deluded as to become incapable 
of estimating facts of their true relations, insist that antisocial acts of 
consumptives should be condoned. However, it is a fact that true 
insanity is extremely rare in tuberculous patients. Working in a 
hospital among patients derived from an ethnic stock peculiarly prone 
to mental alienation, the writer has only twice in twelve years sent 
patients to insane asylums. In private practice also very few of the 
tuberculous patients under the writer’s care became insane. 


1 For literature see Jessen, Lungenschwindsucht und Nervensystem, Jena, 1905. 


CHAP Tie Awe le 
PROGNOSIS IN PULMONARY TUBERCULOSIS. 


The Curability of Phthisis.—Laennec, the first physician to make a ° 
scientific study of the pathology of phthisis, and who really introduced 
physical diagnosis, pronounced it an incurable disease. It appears, 
however, that this keen clinician recognized that many cases do recover. 
He said: “The cure of phthisis is not beyond the powers of Nature, 
but it must be admitted, at the same time, that art possesses no certain 
means of attaining this end.” 

The observations of physicians all through the nineteenth century 
have clearly shown that phthisis is not invariably fatal, despite the 
fact that the treatment applied during the first half of the nineteenth 
century should have killed most of the curable cases, according to 
our understanding of the pathology and therapy of the disease. Still, 
Flint reported 670 cases observed during a period of thirty-four years, 
and the proportion of cases cured or arrested was not much below 
that which we attain at present. Thomas J. Mays! compiled statis- 
tics of Flint’s 670 cases and Williams’s 1000 cases observed for twenty- 
two years, and compared the results with Trudeau’s 1060 cases under 
observation for seventeen years. The percentages of recoveries and 
survivals are about the same, or rather in favor of Flint’s and Williams’s 
cases. 

At present we have sufficient and incontrovertible proof that tuber- 
culosis is curable in all its stages. Experience while making autopsies 
shows, in fact, that it is the most curable of chronic diseases, consider- 
ing the enormous number of persons who show healed, or quiescent, 
tuberculous lesions in the lungs when examined after death. And the 
lesions discovered are often such as to indicate that the process was 
quite extensive at the time of its activity. 

Importance of Prognosis.—There is no need of elaborating on the 
importance of prognosis in the practice of medicine. It is always 
significant and, in the case of tuberculosis, it is, at times, even more 
important than diagnosis. Indeed, most patients come with ready- 
made diagnoses and all they want to know is the ultimate outlook. 
“Will he recover?” is one of the first questions after the patient and 
his friends are told that there is a tuberculous lesion. ‘“‘If so, how long 
will it take till he recovers?”? Moreover, it is important to be ready 
to answer whether the patient, after recovery, will be able to resume 
his occupation, and whether there is danger of relapse. In case of an 


1 New York Med. Jour., 1914, 100, 70. 


PROGNOSIS IN PULMONARY TUBERCULOSIS 619 


unfavorable prognosis it is often asked, “How long will the patient 
last?” 

We cannot answer all or most of these questions in the average case 

with a high degree of certainty. As J. Mitchel Bruce! says: “ Prog- 
nosis in tuberculosis is always a difficult and often a disappointing 
proceeding. With all the facts of a case in our possession the conclu- 
sion we reach proves too frequently to be false. Indeed, paradoxical 
as it may appear, we fail in prognosis most often because of the very 
number, variety, and different character of the facts that we discover. 
Zach of our observations has its own prognostic value, and most of 
them have a different value in different instances and at different times. 
We meet with an extraordinary, variable, and therefore uncertain, 
course of the pathological process from month to month. No disease 
is so difficult to deal with in this connection, and we have to confess 
that we too often find ourselves changing our forecast in both directions 
from time to time.” The extreme difficulty of prognosis in phthisis 
has been best expressed by the one who said that he who attempts to 
forecast the outlook may be sure of one thing only, and that is that he 
will be mistaken. 

The difficulties are, however, not insurmountable in many cases, 
and we can estimate the prognosis of the average patient in any stage 
of the disease with a certain degree of exactitude. But in order to 
do this, we must take into consideration all available facts which may 
have any bearing on the course of the disease. 

Elements of Prognosis in Phthisis.—'The notion that this disease is 
curable only in its incipient stage is one of the half-truths which have 
gained universal credence because of tradition. ‘There are so many 
exceptions as to almost nullify this ancient dictum. We have already 
shown that it is fallacious to classify phthisis into three or four stages, 
and to say, without reservation, that in the first stage it is curable; 
in the second stage the chances of recovery are considerably dimin- 
ished, while in the third stage it is incurable. There are “incipient” 
cases which have no chance, irrespective of the treatment applied; while 
there are many in the third stage whose chances of survival and even of 
efficiency are excellent. For this reason we shall not discuss the prog- 
nosis of phthisis according to the stages of the disease. 

The elements of prognosis in phthisis reside in the following factors: 
(1) The form of the disease; (2) in a given form of the disease, the 
activity of the process as revealed by the constitutional symptoms 
and physical signs; (3) the presence of complications; (4) the extent 
of the lesion in the lungs; and (5) the economic condition of the patient. 

Prognosis in the Various Forms of Pulmonary Tuberculosis.— We 
have seen from our study of the symptomatology of phthisis that the 
form of the disease has a greater influence on the ultimate outlook than 
the extent of the lesion, or even the activity of the process. Thus, 


1 Lancet, 1913, 1, 591. 


620 PROGNOSIS IN PULMONARY TUBERCULOSIS 


in the pulmonary form of miliary tuberculosis, the chances of recovery 
are nil. The patient will die irrespective of the treatment applied. 
In acute pneumonic phthisis the prognosis is very unfavorable, the 
only hope we may entertain is that the disease will take a turn to the 
better, and pursue the course of chronic phthisis. This happens in 
rare instances, but it should not be expec ‘ted in the average Case, In 
fact, we may say that the prognosis is decidedly bad in these cases. 
Patients with acute phthisis usually last as many weeks or months as those 
with chronic phthisis last years. 

On the other hand, taking the other extreme, abortive tuberculosis, 
we find that the prognosis is favorable under all circumstances. Prac- 
tically all patients recover; the vast majority without even knowing 
that they have been tuberculous; or when the disease has been diag- 
nosticated there often remains a lurking suspicion that it was a false 
alarm, even if tubercle bacilli were discovered in the sputum. 

In fibroid phthisis the prognosis is very good indeed, so long as there 
is no fever. The dyspnea and discomfort which this disease causes 
for years are bearable by the average patient. But as soon as fever 
makes its appearance and persists for some time, the prognosis is 
that of chronic phthisis, which will soon be discussed. 

The most important form of phthisis, that of the most common 
chronic type, is the disease in which the prognosis is very difficult to 
formulate in the individual case. We may, be able to prove statistic- 
ally that a certain percentage of cases recover completely; another 
percentage will survive so many years; still another percentage will 
succumb within one or two years, etc. But in the practice of medicine 
we deal with individual cases and statistics often count for naught. 

In the individual case the outcome of the disease depends on so 
many complex and variable factors that it is often very difficult to 
formulate a prognosis. Indeed, we see that the most desperate case, 
slowly or suddenly, with or without any discoverable reason, takes a 
turn to the better and recovers. We see others who drag along for 
years; living, but they do not recover. Still others, in whom the 
general condition has been quite or altogether favorable, suddenly 
take a turn to the worse and the patient is carried off within a few 
weeks or months. 

For these reasons we must enter into the elements of prognosis of 
chronic phthisis in greater detail. 

Age.—The prognosis in children and in the aged has already been 
discussed (see pp. 471 and 477). In adolescents active tuberculosis 
of the lungs is very serious in most cases. If the lesion is extensive, 
and it becomes so in many cases, the outlook for recovery is not bright, 
though not hopeless, in most cases. Especially is this true in tuber- 
culous girls under twenty years of age in whom the disease was preceded, 
or is accompanied, by amenorrhea. On the other hand, in women 
during the menopause the prognosis of tuberculosis is favorable. 
They may remain sick for many years, but they survive for a long time, 


SEX 621 


and may even be fit for ordinary housework, despite the activity of the 
process in the lungs. The common forms of chronic phthisis occur 
mainly during the ages of twenty to forty-five, and the prognosis is to 
be formulated in them by the criteria given in this chapter. 

Prognostic Significance of the Patient’s History.— Many authors 
have stated that patients with a family history of tuberculosis are more 
likely to run an unfavorable course than those derived from non- 
phthisical stock. A consideration of the facts brought together in 
Chapter XX X will show that this is a fallacious view. The patient was 
undoubtedly infected during childhood. Had he suffered a massive 
infection during infancy he would have succumbed to some acute 
form of tuberculosis. The fact that he survived the primary infection 
proves that it was mild; this is also the reason why he now suffers 
from chronic phthisis, and not from an acute form of the disease. 
Indeed, patients showing signs of some local tuberculous lesion at an 
earlier age usually have a slow, sluggish form of phthisis, lasting for 
many years. (See p. 584.) Many authors have calculated that the 
average duration of a phthisical patient with a family history of tuber- 
culosis is longer than of one derived from robust stock. Recent 
medical literature abounds in statistics to this effect. Thus, Noel D. 
Bardswell,! in his statistical study of the patients at the King Edward 
VII Sanatorium, arrives at the conclusion that “having contracted 
tuberculosis, patients with a consumptive family history enjoy the 
same chance of recovery as those who have no such history.” E. 
Arnould? shows that ‘“‘a bad prognosis is relatively infrequent in 
patients with tuberculous parents—that is those who have had oppor- 
tunities in infancy of receiving repeated small doses of infection; it is 
still rarer in those who have themselves previously suffered from some 
clinical manifestations of tuberculosis.’’ The same experience has been 
recorded by Hayek? from statistics gathered in the German army. 
This is also seen in the acuteness of phthisis in persons who have just 
emigrated from rural districts into large cities (see p. 74). 

Experience teaches that the prognosis 1s not different in tuberculous 
adults who are derived from phthisical stock than in those who are not. 
The slight differences that have been discerned appear to be rather in 
favor of the former. 

Sex.—It appears that the prognosis 1s more favorable in women than 
in men. A man acquiring tuberculosis is apt to continue working and 
thus aggravate the prognosis while a woman, who is usually not the 
bread-winner, is more likely to abstain from overexertion, which is 
such an important element in the treatment of this disease. On the 
other hand, pregnancies, labor, and lactations are apt to aggravate 
the prognosis in women. But this factor has been overestimated. 
It appears that the mortality from tuberculosis of women during the 


Med. Research Committee, Special Report Series, No. 33, London, 1919, p. 65. 
Presse Médicale, 1921, 29, 52. 
Miinchen. med. Wehnschr., 1919, 56, 1316. 


ow 


622 PROGNOSIS IN PULMONARY TUBERCULOSIS 


childbearing period of life, fifteen to forty-five, is lower than that of 
men of the same age (see p. 86). Married women are better cared for; 
their husbands work and provide for them, while when the husband— 
the breadwinner—is tuberculous, poverty is inevitable in many cases. 
For these reasons sanatoriums fill more of the male than of the female 
beds. Women are less likely to succumb to some of the more serious 
complications of phthisis, such as hemorrhage, pneumothorax, etc. 
They also less often suffer from laryngeal tuberculosis. 

The Onset of the Disease.—J/n cases with a sudden onset the prog- 
nosis 1s worse than in those in whom the disease came on insidiously. 
Even the fact that the former are more apt to take strong measures 
to prevent the activity of the process does not counterbalance the 
seriousness of an acute onset, excepting when the suddenness refers 
merely to an initial pulmonary hemorrhage. An acute onset means 
severe constitutional and toxic symptoms, low powers of resistance, 
and the process in the lungs extends very quickly, so that in a short 
time quite large portions of one or both lungs are affected. 

Those beginning with hemoptysis have usually a better outlook than 
others. The reason is not clear. Perhaps the dramatic onset frightens 
the patient, and he is apt to institute proper treatment even if he feels 
well after the cessation of the bleeding, while patients with mild 
symptoms, but without hemoptysis, may continue at work till the 
disease is aggravated. But this does not explain all cases. It seems 
that hemoptysis has very often a good influence on the prognosis of 
phthisis at any stage of the disease and many patients feel much better 
after a brisk hemorrhage (see p. 254). The cases marked by an onset 
with pleurisy, dry or moist, have, as a rule, a better prognosis than 
others, as has already been stated (p.515). It has been observed that 
patients who are only slowly regaining their health after an attack 
of pleurisy and are pale and emaciated, are more likely to develop 
active and progressive phthisis than those who recover quickly, and 
soon regain their former health. 

Prognostic Significance of the Activity of the Disease.— We have 
seen throughout this book that the actiwty of the process in the lung 
has a grecter influence on the ultimate outcome than the stage of the 
disease. ‘Lhe activity is best studied by a careful consideration of 
general, or constitutional, symptoms. Of these, fever is the most 
important. There is no active tuberculosis without pyrexia. The 
afebrile cases, discussed elsewhere, are rather uncommon and it is a 
fact that the prognosis is rather good, so long as fever is lacking. Each 
turn for the worse, each complication, is accompanied by a rise in the 
temperature. 

In active disease the prognosis is unfavorable in direct ratio to the 
height and duration of the fever. Every extension of the lesion manifests 
itself by increased pyrexia; persistence of pyrexia, despite rigid rest 
in bed, is pathognomonic of low resistance; the reverse type of fever, 
in which the highest point is reached in the morning instead of in the 


SIGNIFICANCE OF THE ACTIVITY OF THE DISEASE 623 


afternoon or evening, Is of grave prognostic significance—it may be an 
indication of an invasion of both lungs by tubercles. On the other 
hand, moderate fever, less than 101° F. dropping down to normal or 
subnormal in the morning, is rather favorable. In other words: The 
higher the morning temperature, the nearer it approaches the evening 
temperature, the worse the prognosis. Hectic fever, with normal and 
subnormal temperature in the morning, but which rises high in the 
afternoon and evening, is of grave prognostic significance. If it lasts 
for more than a month, the patient will not survive. He may last, or 
even improve for a time, but he will not recover. 

A normal temperature throughout the day and night is a good sign; 
when accompanied by a good appetite, gain in weight, diminution in 
the cough and expectoration, etc., it is an indication of healing of the 
lesion. If fever only ensues after exertion or excitement, the prognosis 
is very good indeed, provided proper treatment is instituted. It is 
for this reason that most who have new and “infallible” remedies for 
phthisis ask for just this sort of cases on which to try the treatment. 
The vast majority recover under any treatment, provided good nourish- 
ment and rest are part of the “cure.” 

Indeed we can, in most cases, formulate our prognosis by a careful 
study of the temperature curve for a few weeks. Of course, we may on 
rare occasions err by putting implicit faith in the temperature curve, 
but the proportion of errors will be less than when we attempt to 
formulate it on other data, especially on the stage of the disease, or 
the findings on physical examination. 

For this reason, @ prognosis in phthisis should not be given after a 
single examination of the patient. It is required that the temperature 
of the patient should be studied for at least two weeks before attempt- 
ing to forecast the outlook. 

The prognostic significance of the pulse should be considered. 
Excepting in heart disease and hyperthyroidism, no disease can be 
evaluated prognostically with the same degree of accuracy by the pulse- 
rate as chronic phthisis. Incipient cases with a pulse not above SO per 
minute have an excellent outlook. Tachycardia is an indication of 
acuteness of the process, or low resistance, or both. Patients who 
have apparently recovered but remained with a rapid pulse have a 
very poor outlook. The outlook is good in chronic cases with slow 
pulse. 

Of the other constitutional symptoms which give us prognostic 
hints, the state of the gastro-intestinal tract is of great importance. 
Patients with good appetite and who digest and assimilate their food 
well, recover, even when they have, for the time being, some fever 
every afternoon. Persistent anorexia and gastro-intestinal disturb- 
ances are of grave prognostic significance. Gain in weight in afebrile 
patients with good appetite is a good sign. But occasionally we meet 
a patient who holds his own, or even gains, despite the fever. In such 
vases the thermometer should be our guide, and not the scale, 


624 PROGNOSIS IN PULMONARY TUBERCULOSIS 


It has been the experience of sanatoriums that patients with positive 
sputum are more likely to have relapses of the disease after their dis- 
charge than those whose sputum has been negative, or became so after 
treatment. Thus at the King Edward VII Sanatorium, Bardswell’s 
statistical studies showed that “the mortality figures indicate that 
cases in which tubercle bacilli have not been demonstrated in the 
sputum enjoy a substantially better prospect than those in which 
diagnosis has been confirmed by this ‘positive’ bacteriological find.” 
While this favorable showing may be attributed to the fact that among 
the “sputum negative” cases a considerable proportion have not been 
tuberculous at all, and a still larger proportion have had abortive 
lesions, still, there is no doubt that the chances of improvement and 
survival are larger in sputum negative cases than in those with 
demonstrable tubercle bacilli. 

Hemoptysis has no influence on the course and prognosis of the disease 
in the vast majority of cases. The initial hemoptyses are rather salutary, 
as was stated above. In the writer’s experience, no patient has suc- 
cumbed to a really initial hemoptysis. Ninety-eight per cent of cases 
of advanced disease recover from hemorrhages. But in cavitary cases, 
which may or may not be doing well, a brisk hemoptysis may unexpect- 
edly kill the patient. In the individual case, if the hemoptysis is not 
accompanied by fever, or the fever lasts only a few days after the 
cessation of active bleeding, the prognosis is good. But if pyrexia 
continues it may point to acute pneumonic phthisis, or to tuberculous 
bronchopneumonia, which is almost invariably fatal. In these cases 
the hemoptysis is indirectly responsible for the fatal issue. 

On the whole, however, patients with hemoptysis have not as good 
an outlook for recovery as those who never bled. Thus, from the 
statistics of Elderton and Perry it appears that “as a whole, the 
mortality among incipient cases which had had hemoptysis was 
considerably heavier than among the cases who had not had it, but in 
the advanced cases the excess was less. Hemoptysis seems to increase 
the mortality in case of male lives, and decrease it in the case of females; 
the difference in the latter case is, however, slight.’’ The statistics 
gathered at Midhurst by Bardswell and Thompson show the same 
results, but they also point to “an initial hemoptysis may be associated 
with a relatively less severe type of the disease.”’ 

The blood-pressure of the patient may give us some valuable prog- 
nostic hints. ‘Those with hypertension have a better outlook for 
recovery than those showing hypotension. Low blood-pressure is 
characteristic of feeble heart action due to the tuberculous toxemia 
acting unfavorably on the cardiac muscle. So long as. the blood- 
pressure remains low, the prognosis is serious. With the improvement 
in the general condition of the patient there is almost invariably 
noted an increase in the blood-pressure. When there appears during 
the course of phthisis an abnormally high blood-pressure, an exami- 
nation of the urine may disclose the presence of albumin and casts. In 


PROGNOSTIC SIGNIFICANCE OF COMPLICATIONS 625 


fibroid phthisis, and in some cases of phthisis in gouty and rheumatic 
individuals, the blood-pressure is normal or above normal and the 
prognosis is good. ; 

Prognostic Significance of Complications.—The presence of com- 
plications, tuberculous and others, modifies the prognosis perceptibly. 
Thus, laryngeal and intestinal tuberculosis aggravate the prognosis. 
Though many recoveries are seen in patients with these affections, 
yet in the individual case we must not give a favorable prognosis in 
those who show positive proof of laryngeal or intestinal complication. 
With advanced laryngeal disease, manifesting itself in aphonia, dys- 
phagia, etc., a fatal issue is to be expected. The same is true of diarrhea, 
which lasts more thana month. We occasionally, however, see patients 
with profuse diarrhea lasting for several months. But they never 
recover. Blood in the stools is another unfavorable sign. Ischiorectal 
abscess is itself an indication of intestinal tuberculous ulceration and 
is of unfavorable prognostic significance. 

Pleurisy is not invariably an unfavorable complication. The dry 
form occurs in nearly all chronic cases and has a rather salutary 
influence on the pulmonary lesion; it is also a good preventive of spon- 
taneous pneumothorax. Pleural effusions are serious, though in many 
cases they have a good influence on the basic disease. We have 
already shown that they occasionally promote the healing of the lesion 
in the lung by compression. But in bilateral lesions the side with a 
free pleura is likely to suffer from an extension of the tuberculous 
process and the outlook is gloomy. 

Empyema isa very bad complication. No recovery is to be expected. 
The patient may last for months, but he will not recover. In exceed- 
ingly rare instances the pus breaks through a bronchus and is expec- 
torated. But even here the ultimate outlook is bad, because of the 
amyloid degeneration of the viscera, and the general malnutrition 
caused by the prolonged suppuration. 

Spontaneous pneumothorax is fatal in 95 per cent of cases within 
one month of its occurrence. The exceptions have already been 
mentioned. 

Tuberculosis of the kidney is of unfavorable import. 

Of non-tuberculous complications we may mention influenza. ‘This 
disease is more often diagnosed in tuberculous patients than facts 
would warrant. An increase in the cough, pyrexia, etc., due to an 
exacerbation of the tuberculous process, is apt to be attributed to 
influenza by patients and physicians. We have already discussed the 
influence of pneumonia on the prognosis of phthisis (see p. 590). 

We often meet other non-tuberculous diseases in patients suffering 
from phthisis. Such as necessitate an operation with the administra- 
tion of a general anesthetic are dangerous, and it has been my rule to 
urge local anesthesia, whenever feasible, in operations on tuberculous 
subjects. But when a general anesthetic is imperative, the outlook 
is not so grave as popularly supposed. Many tuberculous patients 

40 


626 PROGNOSIS IN PULMONARY TUBERCULOSIS 


under my care have been operated upon and held under the influence 
of ether or chloroform for more than an hour, yet they did well after 
recovering from the operation. In most cases the lesion in the lung 
keeps on pursuing its course as if no surgical interference had been 
instituted. C. D. Parfitt reports that 5 per cent of his sanatorium 
patients during seven years had to undergo major surgical operations 
with general anesthesia. Despite the surgical shock and anesthesia, the 
pulmonary condition was not aggravated in any case. Similar experi- 
ences are reported by H. G. Wetherill, of Denver, and H. M. Kinghorn. 
It seems that the entire problem rotates around the activity of the 
pulmonary lesion. An anesthetic administered to a patient with 
extensive lesions in the lungs, running high fever, having a rapid pulse, 
and other symptoms of tuberculous toxemia, will but accelerate the 
inevitable, or aggravate the slight chances of improvement. But when 
the lesion is quiescent, the temperature and pulse around normal, and 
the general condition fair or good, the patient will stand the shock of a 
major operation with general anesthesia. 

Prognostic Significance of Signs Found on Physical Examination. — 
We have already mentioned the fallacy of formulating the prognosis of 
phthisis solely on the findings by physical examination. There are 
cases showing physical signs indicating that we are dealing with 
incipient, or first-stage, cases of the American or Turban classification, 
yet the prognosis is very unfavorable. Indeed, the most wnfavorable 
prognosis should be given in cases showing marked constitutional symp- 
toms which are out of proportion to the findings on physical examination. 

It may be stated that generally the extent of pulmonary involve- 
ment is of more importance than the stage to which the lesion has 
advanced. Cavitation in one lobe is of less danger than infiltration 
of two or three lobes. J. Edward Squire gives the following table 
embracing 2720 cases of phthisis showing the relation of improvement 
to the number of lobes involved: 


Much improved. Improved. Total improved. 
Lobes affected. Cases. Per cent. Per cent. Per cent. 
ee 877 58.38 28.62 87.00 
Ade 1015 37.83 34.67 72.50 
ee DLD 22.52 35:53 58.03 
4. 277 15.16 29.24 44.40 


The fear and apprehension entertained by both the profession and 
the patient for “holes in the lung”’ are based on misconceptions of the 
pathology of phthisis. The fact is that the most dangerous cases of 
progressive phthisis are fatal before cavities are formed. This is the 
case with miliary tuberculosis and, to a certain extent, with acute 
pneumonic phthisis. If a tuberculous lesion in the lung does not cica- 
trize quickly, the best that can happen to the patient is that a cavity 
should form. A pulmonary cavity is proof that the organism is in 
possession of strong powers of resistance, in fact, of immunity; otherwise 
the lesion would spread. The difference between active phthisis with 


SIGNS FOUND ON PHYSICAL EXAMINATION 627 


cavity formation and without such occurrence is analogous to that 
between general septicemia and abscess. In the latter case the disease 
is localized and circumscribed and, when drained, the danger is not very 
great. A cavity has in fact, been defined as a tuberculous abscess 
which is drained through a fistulous opening into a bronchus. 

This is a fact which is not appreciated at present to the extent it 
deserves, though over one hundred years ago that keen clinical 
observer Laennec already spoke of it. Hesaid: “Pretty often, at the 
period when the complete evacuation of a tuberculous cavity is indi- 
cated by the stethoscopic signs, the patient experiences a marked 
jmprovement in his symptoms: the expectoration and fever decrease, 
and, if the improvement only last a little while, even the wasting of 
the body is sometimes diminished. This false convalescence is usually 
only of a few days’ or weeks’ duration; but it may extend to some 
months, and may even seem to be complete. . . . It may even, in 
some rare instances, terminate in a perfect and permanent restoration 
of health.” 

It may be stated that the dangers of tuberculous cavities vary inversely 
with the time vt takes for their formation. The sooner they are produced, 
the worse the prognosis; the slower they develop, the better the ulti- 
mate outlook. In very acute forms of phthisis cavitation is very rare. 
The prognosis is gloomy with or without localized destruction of pul- 
monary tissue. In adults such cases are comparatively rare, but in 
infants rapid cavity formation is seen at times, and the termination is 
almost invariably fatal. In subacute forms of phthisis, in which exca- 
vations are apt to form very rapidly, the prognosis is unfavorable, 
unless the cavity is rather small. In the latter case the disease may 
be attenuated, and subsequently pursue a chronic course with the 
sequestration and expulsion of the affected area. Excavation is then 
the first step toward the diminution of the acuteness of the process in 
the lung. The general symptoms may be ameliorated, as after the 
evacuation of an abscess. 

In chronic phthisis excavations, even when extensive, are compatible 
with a long and efficient fe. ‘These cavities are surrounded by more or 
less dense fibrous capsules which limit their extension, and are drained 
through fistulous tracts communicating with bronchi. So long as the 
secretions are eliminated by expectoration, the patient may feel quite 
comfortable for years. The cavities may even heal, as was already 
shown (see p. 178). When small, they may be obliterated by granula- 
tions or by calcification of their contents. Larger excavations may 
shrink, or even when remaining of large dimensions, they may become 
altogether benign after the necrotic tissue has been expelled. They 
are, however, a constant source of danger of metastatic auto-infection 
or copious hemorrhages. 

In my experience patients with right-sided lesions of this type are more 
likely to recover than those with left-sided lesions. In the former the 
constitutional symptoms, especially dyspnea, tachycardia, etc., may 


628 PROGNOSIS IN PULMONARY TUBERCULOSIS 


improve or disappear after the formation of a chronic cavity and the 
disappearance of the pyrexia. Even dextrocardia may be well borne. 
But in left-sided lesions the heart is pulled over to the left and upward, 
and the patient remains with tachycardia and is distressingly short- 
winded. Pneumothorax ismore likely to occur in the left pleural cavity. 

The rational explanation for the mildness of right-sided lesions as 
compared with those in the left side is this: The left lung is smaller than 
the right and has but two lobes. The division of the lung into lobes 
retards the spread of the tuberculous process—the interlobar fissures, 
lined with double layers of serous membrane, act as barriers. In the 
right lung with three lobes there are two fissures, while there is only one 
in the left lung, and when this is passed, the entire lung is invaded. In 
addition, in extensive left-sided lesions, the diaphragm is drawn upward 
and with it the stomach, while the heart is pulled over to the left 
and upward; in some cases the apex beat may be found in the third 
interspace in the axillary line. The result is almost invariably dis- 
turbances in the circulation due to mechanical causes; the dyspnea 
is severe; more so than in dextrocardia found in right-sided lesions. 
Gastric symptoms, due to displacement of the stomach, are also very 
frequent in extensive lesions of the left lung. While I have seen many 
‘ases with cavities in the right lung and dextrocardia recover, I have 
seen but few with large excavations in the left lung do well. They may 
last for many years, but they are always unable to do anything because 
of severe dyspnea, cyanosis, ete. 

In chronic cases in which the formation of a cavity is slow, the 
prognosis is rather good. In fact, cavity formation, as we have already 
shown, is a sign of immunity. Those with little or no resistance 
succumb before there is an opportunity for cavity formation. 

These cavities are surrounded by dense fibrous capsules which limit 
their progress or extension, and they may be harmless for long periods 
of years. Communicating with bronchi which permit the expulsion 
of the morbid secretions forming on the ulcerated wall, they often 
pursue an apyretic course. Some even have smooth and glittering 
walls without any lymph spaces, and the toxic products within them 
‘annot be absorbed. We meet with cases in which even the tubercle 
bacilli disappear from the sputum and the prognosis is the same as 
in bronchiectasis. 

There are many of this class of patients who, despite having more or 
less extensive excavations, live for many years without pronounced 
inconvenience; in fact, some consider themselves fairly healthy and 
attend to their callings, or even to manual labor. Their main trouble 
consists In a proclivity to “eatch cold,” and only on such occasions 
do they call on their physicians for relief. 

Generally speaking, tuberculous cavities are indications of chronicity 
of the tuberculous process in the lung, showing that the resisting forces 
are active and as such are of better prognostic augury than many active 
incipient cases with pronounced constitutional symptoms. 


SPECIAL TESTS 629 


Patients are to be told that the “holes” in their lungs per se are 
not so dangerous as they believe. That fever, anorexia, etc., are 
more dangerous. They may live and can be active with cavities for 
many years. 

Special Tests.— Various attempts have been made to find tests of 
the severity of phthisis by examination of the blood, urine, etc. We 
have already seen that Arneth’s blood picture is not so reliable as some 
would lead us to believe (see p. 283). Ehrlich’s diazo-reaction was 
at one time considered reliable in indicating the severity of phthisis. 
But it appears that it is positive in cases which are otherwise indicating 
their progressive tendencies. In incipient cases it is, as a rule, negative, 
but I have met with cases in which it was positive, yet the case went 
on to uneventful recovery. It appears that at present very few place 
great reliance on this test. 

Moritz Weisz! found that urochromogen is the principal substance 
which causes the diazo-reaction, and suggested that his test is superior 
to the latter. I used Weisz’s urochromogen test and found it superior 
to the diazo-reaction in indicating the prognosis of active phthisis. It 
is thus performed: Into each of two small test-tubes are put 8 cc of 
urine and 2 ce of distilled water are added; now, to one tube which is 
to be tested for urochromogen, 38 drops of 1 to 1000 solution of potas- 
sium permanganate are added, the tube is shaken thoroughly and com- 
pared with the control tube. The appearance of the faintest yellow 
color shows the presence of urochromogen and is easily detected by 
comparing with the control tube, to which no potassium permanganate 
is added. The test is read positive, however, only when the solution 
stays clear. 

In this country Heflebower,? and J. Metzger and S. H. Watson® 
have reported that this test is a reliable guide in estimating the activity 
of the tuberculous process and gives indication as to prognosis. I 
find that it is positive during acute exacerbations of the disease and 1s 
usually negative in incipient, or even in quiescent, cases. In acute 
progressive cases it is found positive, and it becomes more and more 
intense with the extension of the disease. It is negative in most 
favorable cases. 

The complement-fixation test, which has of late been used in the 
diagnosis of tuberculosis with doubtful results (see p. 392), has been 
found by some authors to have some prognostic value. Debains 
and Jupillet report that in active incipient and hopeful cases of phthisis 
the reaction is usually positive, while in advanced cases with pro- 
nounced emaciation the reaction is often feeble or altogether negative. 
They try to explain these phenomena on the assumption that in pro- 
gressive and advanced phthisis the antibodies in the serum have already 


Miinchen. med. Wehnschr., 1911, 58, 1348. 
Am. Jour. Med. Sci., 1912, 143, 221. 
Jour. Am. Med. Assn., 1914, 62, 1886. 
Compt. rend. Soc. de biol., 1914, 76, 199. 


eon 


630 PROGNOSIS IN PULMONARY TUBERCULOSIS 


been bound or neutralized by the substances produced by the tubercle 
bacilli. They also found that in experimental tuberculosis in rabbits 
complement-fixation activity goes hand-in-hand with the resistance of 
the animal. On the other hand, in tuberculous pleurisy with effusion 
negative reaction was mostly found, and this form of the disease 
cannot be considered as of especially unfavorable prognosis. In fact, 
we have shown that the outlook in pleurisy is rather bright. Most of 
the work along these lines was done by Besredka,! who reported that 
the reaction is uniformly positive in early cases of phthisis; in moder- 
ately advanced cases it is positive in the majority. With the advance 
of the disease the reaction becomes feeble, and finally in the terminal 
stages of phthisis it becomes negative. With Manoukhine he regards 
a negative reaction in advanced phthisis as a sign of approaching death. 

From the results obtained by H. R. Miller in my wards at the 
Montefiore Hospital, the complement-fixation test showed no indica- 
tions that it may be utilized for prognostic purposes. It has been 
found positive in active, as well as in quiescent, or healed cases, and as 
often negative in cases in which the contrary might have been expected. 

Influence of Economic Conditions of the Patients on the Prognosis. — 
The occurrence of phthisis is in itself an indication of poverty. To 
be sure, we meet with numerous rich consumptives, but economic 
prosperity is not always an indication of rational life, proper food, 
regular hours, avoidance of physical and mental overexertion, etc. 
But in a given case of phthisis the prognosis is often influenced more 
by the social and economic condition of the patient than by any other 
single factor. After all, phthiszs 1s the most expensive of diseases because 
it disables the patient for a long period of time and requires costly 
treatment, including nourishment, a favorable home, etc. 

The patients who can afford to bear the expense are more likely to 
recover than those who cannot. The artisan often has a family depend- 
ing on him for support, and he is likely to keep at work while sick, till 
the disease has progressed to a stage where he can do no more, and drops 
from sheer exhaustion. It is in these cases that the institutions, as well 
as the social service of modern enlightened communities, do consider- 
able to improve the prognosis of phthisis. But it must always be borne 
in mind that these agencies can do much better than merely give advice 
about the dangers of living with tuberculous persons, and distribute 
scare head literature and sputum cups. If they do only this, the prog- 
nosis is often aggravated because the patient is, at times, treated like 
a pariah by his relatives and friends who are frightened by the numer- 
ous “visitors,” the social workers, nurses, physicians, and others. I 
have seen families broken up in this manner; families in which there 
were no infants, and there was no reason to fear dissemination of the 
disease. But what is of most importance, the patient, deprived of the 
comfort of a good home, becomes despondent and the lesion progresses 
more quickly than it would otherwise. 


1 Ann. de l’Inst. Pasteur, 1914, 28, 569; Compt. rend. Soe. de biol., 1914, 86, 197. 


PROGNOSIS IN ARRESTED DISEASE 631 


Prognosis in Arrested Disease.—We have seen that only lesions 
of abortive tuberculosis are completely healed by cicatrization and 
calcification. But this form of the disease is not recognized, as a rule, 
during its activity and the prognosis is good at all events. It is 
different with chronic phthisis which has ‘Tasted for some time and 
finally there is an abatement in the constitutional symptoms and the 
patient is considered cured. 

Cure by restitutio ad integrum is out of the question in these cases. 
The cicatrized and calcified foci usually contain virulent tubercle 
bacilli which may at any time become active again, flaring up the lesion 
or causing metastatic auto-infection. Experience has taught that in 
the vast majority of cases these patients attain but “quiescence,” and 
the term “arrested disease,’ which has recently been substituted for 
the term “cured,” which was formerly in vogue, is proper. The 
patient is justified in asking for an opinion whether this arrested con- 
dition is likely to be lasting, or whether he will sooner or later suffer 
from a recrudescence of the symptoms of phthisis, a relapse which is, 
in fact, an acute or subacute exacerbation. In other words, is the 
arrest of the disease an indication of a more or less permanent freedom 
from tuberculous sickness or is it merely a long remission in the progress 
of the disease? 

These problems can be solved, in many cases, by a consideration of 
the physical signs found in the chest, but with greater certainty when 
the constitutional symptoms are considered. 

Physical exploration of the chest discloses usually signs of cicatriza- 
tion of the involved lung tissue, pleural adhesions, ev idence of fibro- 
sis, while the rest of the lung may show indications of emphysema. 
Adventitious sounds are isually, though not invariably, absent; the 
case is “dry.” Exquisite amphoric breath sounds may be heard over 
the site of ras combined with amphoric whispered voice, but no 
rales. In others, the site of the lesion is only discovered by the dulness 
on percussion, and feeble breath sounds and sibilations are found over 
a circumscribed area of the chest, usually the upper part of one side. 
In many there are found signs of displacement of the mediastinum. 
But we have already emphasized the fact that the physical signs 
elicited on the chest are of but little value prognostically. The writer 
is under the impression that a patient showing a well-defined line of 
demarcation between the normal lung and the affected part has a better 
prognosis than one showing a gradual change from normal to pathological 
lung tissue. But to this there are many exceptions. 

The problems, “ Will the quiescence last?” and “Is the patient in 
danger of a relapse of the disease?’’ can best be answered by a careful 
consideration of the constitutional symptoms. In general terms it 
may be stated that the patient is in danger of two accidents: (1) 
pulmonary hemorrhage; and (2) reactivation of the disease. 

Pulmonary hemorrhage cannot be foreseen in these cases, nor can 
it be prevented. It may occur when the patient is in excellent condi- 


632 PROGNOSIS IN PULMONARY TUBERCULOSIS 


tion. When not copious, it merely frightens him, but even brisk and 
copious hemorrhages are well borne by 98 per cent of patients; in 
fact, they feel better in many cases after recovery from the bleeding, 
and quickly recuperate. Some have one such large hemorrhage a 
few years after recovery from phthisis and feel well for many years 
thereafter, or even for the rest of their natural lives. But in about 2 
per cent of these bleeders the hemorrhages prove fatal. As was already 
stated, these hemorrhages cannot be foreseen nor prevented. ‘Those 
suffering from “recurrent hemoptysis” hardly ever perish because 
of the bleeding. The danger is a brisk hemorrhage occurring suddenly 
in one who may not have bled before. 

An exception is, however, to be made in the case of streaky sputum. 
In many patients with well-healed lesions in the lungs, minute hemor- 
rhages occur, especially after slight exertion, or acute non-specific 
infections of the upper respiratory tract, etc. So long as there is no 
fever, severe cough, etc., this is to be considered capillary hemor- 
rhage, due to ruptures of minute bloodvessels in the sclerosed pul- 
monary tissue. These slight attacks of hemoptysis are a good sign of 
healing, and should not alarm the patient. It is different with copious 
attacks of hemoptysis of which we spoke above. They are liable to 
threaten life in rare instances. 

Healing of the tuberculous process in the lung frequently leaves the 
patient with certain annoying symptoms for an indefinite time. Many 
have pains in the chest, which may be aggravated during meteoro- 
logical changes. This is particularly observed in patients who have 
pleural adhesions. In some the pain is paroxysmal, coming on without 
any known provocative cause, lasting for several days, and disappear- 
ing. No lasting improvement can be attained by therapeutic inter- 
vention. But the patient may be assured that these pains are no 
indication of a recurrence of the tuberculous process, so long as there is 
no elevation in the temperature or an acceleration in the pulse rate. 

The constitutional symptoms are better guides in prognosis as to 
the chances of a lasting quiescent period. Most of these patients 
with arrested phthisis remain emaciated, anemic, with wasted muscles, 
often presenting a cadaverous appearance. Despite this, many of 
them are very active at their avocations and, in fact, they display 
energy and perseverance which is surprising when considered in connec- 
tion with their physical decrepitude. Some are rather well nourished 
despite the fact that physical exploration shows a lesion of various 
degrees of activity, from cicatrization to excavation. In my expe- 
rience, patients apparently well nourished, with quiescent or arrested 
lesions of this class are not as a rule doing as well as those of the lean 
type, despite their well-nourished bodies. We should not allow our- 
selves to be deceived in attempting a forecast by the amount of fat the 
patient has, by the fresh and browned skin which is often merely a 
superficial mask of improvement, while the interior of the organism is 
vitally undermined. 


PROGNOSIS IN ARRESTED DISEASE 633 


The prognosis in these two classes of patients can only be determined 
with some degree of certainty by an analysis of the following condi- 
tions: If the improvement has been attained through careful treatment in 
a favorable environment, the test is whether the patient remains in good 
condition for some time after returning to his old environment without 
suffering a relapse of the constitutional symptoms. The test, in other 
words, is duration; improvement counts if it lasts without special 
treatment. 

So long as there is but little cough, or none at all, no fever, no tachy- 
cardia, dyspnea, chills, sweats, etc., the prognosis is good, no matter 
what physical exploration discloses. Continuous freedom from these 
symptoms for several months is an indication of arrest, even if tubercle 
bacilli are found in the sputum, while in those in whom arrest has just 
been attained, the prognosis is uncertain until time has shown that 
there is no tendency to recrudescence. The prognosis is even better 
in those who, despite resumption of their previous occupation or taking 
up a new one, and living a rational, though not an exceptionally 
careful life, still keep in good condition. On the other hand, in those 
who purchased quiescence or arrest of the disease by special treatment, 
rest, and extreme care, the prognosis vs less favorable, unless resumption 
of ordinary activities of life proves that recrudescence does not occur. 

In short, the prognosis of quiescent and arrested disease can only 
be made by a careful observation, for several months, noting the effects 
of resumption of activities of life on the condition of the patient. 


COBPA\P GBR xen 


THE MEDICO-LEGAL AND INSURANCE ASPECTS OF 
TUBERCULOSIS. 


Lastina for many years in most cases, tuberculosis disables the 
patient more or less during the period of illness. If he has been insured 
in one or more of the corporations, or fraternal organizations which 
guarantee a certain sum per week or month for loss of working or 
business time owing to disability due to sickness, the physician must 
certify as to the ability of his patient to attend to his vocation. With 
the modern methods of workmen’s insur ance, it may be alleged that the 
victim of tuberculosis has acquired the disease as a result of the nature 
of his work, or because of lack of precautions to prevent the spread and 
development of tuberculous disease, and thus the question of com- 
pensation arises. Numerous men, having served in the army during 
the war, are now being cared for by the Gaverawient because of their 
disability due to tuberculosis acquired during or soon after, military 
service. In these cases, examining physicians have to determine the 
lability of the Government, the extent of the disability, ete. Tuber- 
culosis begins in most cases ingidiotsly and there is time for the patient, 
knowing his condition or not, to apply for life insurance, and it is the 
province of the physician acting as examiner for the insurance corpora- 
tion, to detect the disease, even though the applicant gives him no clue 
as to constitutional symptoms. Very frequently claims for damages 
are brought in courts because of actual or alleged traumatic origin of 
pulmonary tuberculosis. Expert medical testimony is then sought 
to advise the court whether, in the given case, the tuberculous process 
in the lungs may be charged to the injury. These and kindred subjects 
will be discussed in this chapter. 

Disability Resulting from Tuberculosis.—The acute and progressive 
forms of the disease clearly disable the patients and no question can 
arise as to the patient’s ability to work or attend to his business. The 
fever, cough, emaciation, weakness, etc., are self-evident and, as a rule, 
the insurance company or fraternal organization will not contest the 
claim for payment of the benefit promised in the contract. 

It is different with the chronic forms of tuberculosis. These, as 
has been shown throughout the clinical parts of this book, are charac- 
terized by an undulating course, with exacerbations and remissions in 
the activity of the disease. The problem then arises as to the ability 
of the patient to work and the liability of the company. It seems that 
health insurance companies, once they are satisfied that the diagnosis 
of pulmonary tuberculosis is correct, especially when tubercle bacilli 


DISABILITY RESULTING FROM TUBERCULOSIS 635 


have been demonstrated in the sputum, raise no more the question as 
to the disability and its extent and, as a rule, keep on paying the 
benefits. The writer knows of a case in which the insurance company 
settled with a policyholder for a flat sum believing that with tubercle 
bacilli in the sputum recovery is unlikely. The policyholder, how-— 
ever, soon became aware of his ability to work and has been doing so for 
two years. 

In attempting to decide as to ability to work of tuberculous policy- 
holders the physician should be guided mainly by the constitutional 
symptoms, while signs elicited while exploring the chest should be given 
a subordinate position. In some cases the general appearance of the 
patient is sufficient to decide. Those who are evidently emaciated 
and weakly, with a hectic flush, ete., can be put down as disabled. 
The examination of the chest is then made for the purpose of ascertain- 
ing the cause of the disability, and the extent of the lesion in the lung. 
In most cases a detailed examination is necessary before we can arrive 
at a decision as to the extent of the lesion and the outlook for recovery. 
It may be stated that a patient with a tuberculous lesion in the lung 
who has fever above 99.5° F. by mouth, or 100° F. by rectum, is not 
fit for work of a remunerative kind. There are many exceptions, to be 
sure, and they have been discussed in Chapter IX, but when an 
insurance policy is involved, disability must be considered complete in 
these cases for the time being. Likewise, those with tachycardia, with 
a pulse rate of 90 and more per minute, even when afebrile, must be 
considered disabled. In many instances functional tests must be 
applied, such as exercise of a more or less vigorous nature before the 
real character of the disability is ascertained. If, after performing 
some task, such as walking one or two miles, or working at the policy- 
holder’s occupation for an hour or two, the pulse, temperature and 
respiration remain normal, the individual may be considered fit for 
work; at most, payment for partial disability may be allowed. Of 
course, when these persons with dormant, or quiescent tuberculosis 
begin to work, it is imperative that they continue under medical 
supervision for several months, reéxamined at first once a week for two 
or three months, then monthly, and when it is found that work for a 
year has not deleteriously influenced the weight, temperature and 
pulse rate, they may completely be discharged with the admonition 
that with the first appearance of symptoms they must report for 
reéxamination. 

It will be noted that cough and expectoration have not becn men- 
tioned among the constitutional symptoms which are invariably dis- 
abling. Many tuberculous individuals who have completely recovered 
remain with more or less cough; some even expectorate mucous 
or mucopurulent material for years, or indefinitely, but they remain 
strong, and well able to pursue their vocations. Even the finding of 
tubercle bacilli in the sputum is not inconsistent with ability to gainful 
employment in some cases. Likewise, the signs elicited on physical 


636 MEDICO-LEGAL AND INSURANCE ASPECTS 


exploration of the chest are not reliable criteria per se as to disability. 
In many instances it will be noted that, despite the unmistakable 
signs of extensive involvement of the lung, even of excavations, the 
general condition of the patient suffers but little, if at all; this may be 
seen in patients with cavities which cannot be considered “dry.” On 
the other hand, in many cases in which the physical signs indicate but 
slight or even doubtful lesions, the constitutional symptoms are so 
pronounced as to completely disable the patient. The same may be 
said about roentgenographic findings. They merely indicate ana- 
tomical changes. But whether the changes disclosed on the plate are 
active, or disabling, cannot be determined with exactitude in every 
case merely by an examination of the roentgenogram. In fact, 
healed, cicatrized lesions at times cast a more pronounced shadow than 
some active lesions. Here, again, only constitutional symptoms decide. 

Hemoptysis, especially the form in which the sputum is merely 
streaked with blood, cannot be considered as completely disabling, 
when there are no other symptoms of active disease. We have shown 
that recent investigations have demonstrated that exertion is hardly 
ever responsible for bleeding from the lungs (see p. 242); we have also 
seen that in some instances in which the lesion is, for practical pur- 
poses, cicatrized, the patients keep on expectorating blood-streaked 
sputum at irregular intervals for many years without reactivation of the 
process in the lungs (see p. 632). In some cases with cavities more or 
less profuse bleeding may occur, and soon after the hemorrhage ceases, 
the patient feels well, or even better than before the accident. Such 
hemorrhages should be judged by the after-effects. If, after the 
bleeding has ceased, the temperature and pulse rate are normal, and 
the patient regains the loss of blood and weight he sustained during 
the hemorrhage, he is often fit for resuming his occupation. Over- 
exertion and excitement are hardly ever a cause of copious, or fatal 
hemorrhages, though they may be coincidental, and for this reason 
they have been exploited by writers of fiction, and on the stage. 

The dangers of reactivation of healed tuberculous lesions as a result 
of moderate exertion have been greatly exaggerated by physicians and 
patients especially in health resorts and sanatoriums. No claim can 
be made to the satisfaction of careful clinical observers that patients 
with inactive or healed lesions, who keep at perfect rest have no relapses 
indefinitely. One has to scrutinize carefully the histories of patients 
who had been at rest in institutions for many months, or years, and it 
will be observed that, despite the rigid rest cure, reactivation occurs 
now and then without any discoverable causes. The psychic factor 
must be borne in mind, especially when dealing with patients who have 
been thoroughly institutionalized, in either public or private and expen- 
sive sanatoriums. They often become psychasthenic, introspective, 
and lazy; they have acquired the “thermometer habit,’ and cannot 
be weaned from it; they suffer from “hemophobia”’ (see p. 248), and 
fear the least exertion. They are difficult to manage and fraternal 


DANGERS OF INFECTION 637 


organizations have them on their hands indefinitely. Recently the 
Government has had quite some trouble with this sort of cases among 
ex-service men. 

Of course, in many of these healed or arrested cases of tuberculosis 
complete rehabilitation is not attained, and allowance for partial 
disability is to be considered. This is seen in patients in whom the 
lesion has healed excellently, but sclerosis of the affected lung tissue, as 
well as pleural adhesions, cardiac displacements, etc., leave him short- 
winded, with cyanosis of the lips and fingers, pains in the chest, ete. 
They may last for many years, perhaps their natural duration of life, 
and when they finally succumb, death is due to some other disease. 
But they lack endurance while they live. They cannot be considered 
rehabilitated, even though the lung lesion is practically healed, perhaps 
even better than in others in whom the disability is slight, though the 
lesion is apparently active or at most quiescent. It is in these cases 
in which the judgment of a physician with extensive experience with 
tuberculous patients is important when the problems of sickness, 
insurance or the liability of the Government to ex-service men are 
considered. Each case should be judged by itself. But in this, 
individualization, the reaction of the body to work, functional tests in 
other words, should be the basis for an opinion, and here again the 
temperature, pulse-rate, etc., are the criteria. 

Nature of the Occupation.—Insurance companies assure an income 
for loss of business time, or inability to pursue a gainful occupation, 
because of sickness. Some occupations are completely barred to those 
who have had tuberculous disease. Among these are such as require 
strong muscular exertion, dusty trades, or those necessitating exposure 
to the vicissitudes of the weather. It is, in fact much safer for these 
persons to work indoors, provided the workshop, factory or mill is 
well ventilated and lighted. Guided by the principles laid down in 
Chapter XX XV, the medical examiner for insurance companies and 
fraternal organizations may be in a position to determine the hazards 
of working at most occupations. 

Dangers of Infection.— The dangers of infection of fellow-workmen, 
which at times have been invoked by those who claim compensation, 
are to be disregarded. The number of “carriers” of tubercle bacilli 
is so large that the task of separating them from non-carriers cannot 
be attempted, and could not be accomplished even if attempted, with 
all the powers of the Government. Moreover, we have shown that 
there is no danger for adults because they have practically all been 
infected during childhood, and that this early infection gives them a 
certain degree of immunity against renewed and exogenous infection 
with tubercle bacilli (see Chapter V). Of course, in cities in which the 
health officers prohibit patients with a history of tuberculous disease 
from working at certain occupations, mainly involving the handling 
of food and food products, a change of occupation may be necessary 
in some instances. 


638 MEDICO-LEGAL AND INSURANCE ASPECTS 


TRAUMATIC TUBERCULOSIS. 


Injury as a Cause of Extrathoracic Tuberculosis.— That traumatism 
may determine the localization of extrathoracic tuberculous lesions— 
of bones, joints, glands and meninges—is a well-known and accepted 
clinical fact, supported by animal experimentation. A considerable 
amount of information on this subject may be found in the works of 
R. Stern,! A. Ascarelli,? F. Parkes-Weber,? Léon Giroux,’ H. Grau, 
and many others. There appears, however, a considerable difference 
of opinion as to the frequency of traumatic tuberculosis in daily medical 
practice. Giroux collected the following figures as to the frequency 
of traumatism as a cause of surgical tuberculosis: Jeannel found that 
5 per cent of cases are post-traumatic; Wilner, 6 to 7 per cent; Pietrzi- 
kowski, 8 per cent; Lemgey, 8.81 per cent; Estor, 9.5 per cent; Hahn, 
31 per cent (of hip-joint disease); Honsele, 44 per cent; Kénig, 20 per 
cent; Voss, 21 per cent; Horzetzky, 44 per cent (tuberculosis of the 
vertebrae); Taylor, 52 per cent; and finally Bauer, almost 100 per cent. 

The differences in the percentages, running from 5 to nearly 100 per 
cent, show that some writers have greatly exaggerated the role of trau- 
matism in the etiology of surgical tuberculosis. Indeed, many recent 
writers are inclined to the opinion that only in exceptional cases is 
traumatism responsible for the development of tuberculosis of bones 
and joints. Inasmuch as these forms of tuberculosis occur mainly in 
children, it is clear that an inquiry will nearly always elicit a history 
of an injury, usually a slight one, because but few children pass through 
a day or a week without hurting themselves in some manner. More- 
over, the symptoms coming on insidiously, the child may only begin 
to complain after some injury and thus mislead the parents and the 
surgeon into the belief that the tuberculous lesion was the result of an 
injury. 

As traumatic tuberculosis may be considered lesions resulting from 
inoculation of the tuberculous virus into the skin, such as the pathol- 
ogist’s and the butcher’s warts, as well as the rare cases of infections 
when an open wound is inoculated accidentally while breaking a sputum 
receptacle, etc. But, as was already shown, these are extremely rare 
cases. An injury inflicted with a blunt instrument and causing merely 
a contusion, cannot produce tuberculous disease, unless there are 
tubercle bacilli somewhere in the body. However, in the light of our 
present knowledge of phthisiogenesis, it is clear that many, if not 
most, persons harbor some latent or healed tuberculous foci with 
virulent tubercle bacilli, which an injury may reawaken into activity. 
Reducing the vitality and resisting powers of the tissues at the injured 


1 Ueber traumatische Entstehung innerer Krankheiten, Jena, 1910. 
2 Policlinico, 1907, 14, 1025. 

3’ Traumatic Pneumonia and Traumatic Tuberculosis, London, 1916. 
4 La tuberculose pleuro-pulmonaire traumatique, Paris, 1915. 

5 Handbuch d. Tuberkulose, 5, p. 69. 


TRAUMATIC TUBERCULOSIS 639 


point, hematogenous or lymphogenous metastatic localization of 
tuberculosis is favored. 

Traumatic Pulmonary Tuberculosis.—It has been known for a long 
time that injuries to the chest may favor the development of pulmonary 
tuberculosis. Goethe attributed his pulmonary hemorrhage at eighteen 
years of age to overexertion and a fall from a horse. But very few 
authentic cases were observed during the past century; Grasser could 
find reports of only 50 cases before 1903. In the Prussian army it was 
observed that among 6924 cases of phthisis, 95 began after injuries, 
and of these 79 had sustained contusions of the chest. This would 
indicate that it is more frequent than was formerly appreciated. 

It is clear that primary tuberculosis cannot be caused by an injury 
to the chest. The only explanation we can offer for tuberculosis 
following traumatism is that after a contusion of the lung, the pulmo- 
nary tissue is devitalized so that tubercle bacilli brought in with the 
inhaled air will find a suitable soil for growth. Theoretically this 
mode of origin is possible. But to prove such a case it is necessary 
that a new lesion should be found during an autopsy, while careful 
search should fail to reveal old tuberculous foci anywhere else in the 
body. According to Grau such a case has, so far, not been reported. 
But many cases have been observed in which latent tuberculous 
lesions in the lungs, or other organs, have been stirred into activity 
soon after injuries. Inasmuch as we may confidently state that practi- 
cally everybody has been infected with tubercle bacilli at some period 
of his or her life, but that in the vast majority of people this infection 
proves harmless, it is clear that, for medico-legal purposes, active 
tuberculosis following an injury should be considered a valid cause for 
claims for damages when an attempt is made to determine the respon- 
sibility. 

In persons known to be tuberculous the disease may be aggravated 
by an injury, as the writer has seen in many instances, and lead a 
mild case to a rapidly fatal termination. Especially is this true when 
hemoptysis is caused by the injury. While in the usual hemorrhage 
from the tuberculous lung recovery is, as a rule, rapid, the blood soon 
regenerates, and the patient often feels even better than before the 
bleeding occurred, it is different when an injury is the cause of the 
hemorrhage. In such cases we usually deal with a contusion of pul- 
monary tissue, which prepares the soil suitable for the growth of 
tubercle bacilli, involving extension of the morbid process in the lung. 
Traumatism may also produce pleurisy, usually dry, but occasionally 
with an effusion. Pneumothorax is another possible result of an 
injury to the chest. In non-tuberculous pneumothorax the rent in the 
visceral pleura heals more or less quickly and the air is absorbed. 
Effusions in these cases are usually serous or serosanguineous, and are 
also absorbed. Even pyopneumothorax in a non-tuberculous individual 
is usually cured by surgical intervention. But in those with pre- 
existing tuberculous lesions in the lungs or pleura, active or dormant, 


640 MEDICO-LEGAL AND INSURANCE ASPECTS 


the course of tuberculous pneumothorax, hydrothorax, pyopneumo- 
thorax, etc., may be followed. The prognosis in these cases is very 
grave (see p. 533). When the ribs are fractured, which is not uncom- 
mon in these cases, interstitial emphysema, subcutaneous and medias- 
tinal, may occur and mediastinal emphysema may prove fatal in rare 
instances. 

Intensity of the Injury.—The intensity of the injurv should not be 
taken as a measure of the probability of its relation to phthisis subse- 
quently developed, as has been pointed out by many writers. After 
violent injuries to bones and joints, especially those resulting from 
fractures, tuberculous osteomyelitis is hardly ever observed. During 
the World War very few eunshot wounds of bones and joints, and 
especially of the chest, were followed by tuberculous lesions in these 
tissues. On the other hand, slight injuries to bones have frequently 
been seen to precede tuber enlous osteomyelitis. In the same manner 
the writer has seen in several cases a a slight i injury to the chest flaring 
up a latent, or quiescent tuberculous process in the lung. In persons 
known to be healthy, this is not uncommon. John B. Hawes! points 
out that after the autumn football season some players develop con- 
sumption as a result of injuries received on the football field. The 
special diet usually prescribed by the trainer, as well as the excessive 
exertion for months during the training period, undoubtedly reduce 
the resisting powers of even gridiron heroes. Parkes-Weber says: 
“Muscular men, such as athletes, runners, football players, boxers, 
and persons who live healthy, open-air lives and who, owing to their 
splendid physique, might be supposed to be specially resistant toward 
tuberculosis (but are, it must be remembered, peculiarly liable to con- 
tusional injuries and strains), sometimes surprise every one by more or 
less suddenly falling victims to tuberculous affections, especi ially of the 
lungs. W hen one hears of vigorous men, living ‘healthful’ open-air 
lives, becoming victims of pulionany or other kinds of tuberculosis, 
one should always remember the possibility of some sort of traumatism 
having played a part in the etiology. . . . Onsome parts of the 
continent bargemen, who push their chests against poles, ete., are, I 
believe, said to be peculiarly liable to pulmonary tuberculosis.” In 
this country tuberculosis often terminates the career of well-known 
athletic men. 

Clinical Aspects of Traumatic Tuberculosis of the Lungs.—'The site 
of the lesion in the lung provoked by an injury is not necessarily 
at the point affected by the blow. Many have observed lesions by 
contrecoup. In rare cases acute general miliary tuberculosis results 
from breaking up of a latent lesion and flooding tubercle bacilli into 
the blood stream. Hemoptysis immediately following the injury is 
not absolutely essential to establish the relationship between the 
injury and the disease, for laceration of the lung may occur without 


1 Boston Med. and Surg. Jour., 1913, 168, 83. 


TRAUMATIC TUBERCULOSIS 641 


causing hemorrhage. When hemoptysis occurs, as it does in many 
cases, the quantity of blood expectorated is no criterion of the size 
of the torn vessel, or the extent of the area of lung tissue contused. 
Nor must there remain any external marks on the chest wall because 
an injury may lacerate the lung without leaving any external traces. 

The appearance of clinical symptoms of phthisis may be delayed 
for some time. In cases of quiescent lesions which are activated 
as a result of traumatism, the aggravation in the condition of the 
patient, and the extension of the process, may appear soon after the 
accident, and hemoptysis may appear even immediately. In many 
cases the bleeding is, however, delayed several hours or days, which is 
to be expected considering the pathology of hemoptysis. In appar- 
ently healthy persons the symptoms of phthisis may appear many 
months, or even years, later. Hawes reports several cases in which 
phthisis developed from two to ten years after the injury. The writer 
has givey testimony in similar cases. 

The appearance of demonstrable tubercle bacilli in the sputum may 
be delayed for weeks and months, and this does not militate against 
the traumatic origin of the disease. We know that in many cases of 
spontaneous phthisis bacilli are found only months, or even years, 
after the onset of the disease. 

It takes about eight weeks for a tubercle to develop, and one tubercle 
is by far not enough to give symptoms or signs by which it can be 
recognized by the patient or the physician. In fact, when a few days 
after an injury signs of phthisis are found, especially tubercle bacilli 
in the sputum, we may conclude that we are dealing with a preéxisting 
lung disease which, at most, has been aggravated by the accident. 
But in cases in which the symptoms, such as fever, emaciation, cough, 
expectoration, etc., make their appearance three to six months after 
the injury, in a person known to have been well before the accident, 
and the physical signs of the local lesion appear even later, it is obvious 
that there was a causative relation between the injury and the disease. 
German authorities have limited the time for the appearance of 
symptoms after an injury to six months, although there are undoubtedly 
exceptions which must be judged on individual merits. It appears 
that in our army we recognize responsibility for several years, inasmuch 
as it appears to be the policy of the Government to care for tuberculous 
veterans for years after discharge from the service. 

In many cases symptoms of acute pleurisy make their appearance 
within a few days—chilly sensations, fever, pain in the chest, dyspnea, 
ete. Usually these disappear within a few days, and are later followed 
bs «symptoms of phthisis. In some instances there occurs a pleural 
effusion which runs its course In the same manner as the average case 
of this type not due to traumatism, unless it is due to a rent in the 
visceral pleura with resulting hydro- or pyopneumothorax. With 
fractures of ribs, subcutaneous and mediastinal emphysema may occur 
in addition to pneumothorax. Hemoptysis has not been frequent in 

4] 


642 MEDICO-LEGAL AND INSURANCE ASPECTS. 


cases observed by the writer, excepting in those who had suffered from 
pronounced phthisis for some time before the accident and the 
traumatism was the exciting cause of the hemorrhage. In such cases 
the amount of blood lost may be considerable. In most instances the 
hemoptysis Is rather slight, a few mouthfuls, or merely streaky sputum 
is brought up. 

Physical exploration of the chest may disclose the lesion right under 
the site of the injury on the chest, but at times it is found far away from 
it, even in the opposite lung, by contrecowp, as was already stated. 
This is an important point in cases in which responsibility for the 
disease must be established. In several cases of basal phthisis, the 
lesion being located in one of the lower lobes of the lung, I found it due 
to injury. In one instance it was a kick with the hoof of a horse; in 
another, a fall on the side sustaining a contusion of the chest; in still 
another the rebound of the crank while starting an automobile injured 
the chest. 

The course of the disease may be acute, subacute, or chronic, and 
any of the clinical forms of tuberculosis may be observed. In fact, 
there is hardly any difference to be discerned in this regard between 
traumatic and spontaneous phthisis. The outcome depends mainly 
on the resisting powers of the patient. 

The writer has observed several cases of acute miliary tuberculosis, 
and acute pneumonic phthisis following injuries. In such cases it was 
clear that the injury was inflicted on some part of the body in which 
there was a quiescent, or dormant tuberculous process. In one 
instance the patient was struck with a bottle over the chest. He 
immediately had a copious pulmonary hemorrhage, and within twenty- 
four hours the temperature rose to 104° F. and kept at this level for 
about six weeks, accompanied by symptoms and signs of acute pneu- 
monic phthisis, terminating fatally. I. Parkes-Weber reports a case 
in which an injury set free a caseous focus in the epididymis, producing 
fatal phthisis. In fact, injuries to tuberculous testicles are very 
frequently followed by acute miliary tuberculosis with meningeal 
complications, as has already been shown (see p. 588). 

Surgical Operations.—The development of acute and progressive 
tuberculosis after surgical operations may be classed with traumatic 
tuberculosis. This is mostly seen after operations for some chronic 
tuberculous disease of a joint, bone or gland which is followed by 
symptoms of acute miliary tuberculosis and ends fatally. The writer 
has seen cases of this sort develop after bloodless operations and 
manipulation of joints, and Parkes-Weber,’ Urban,’ Orth,’ and others 
report similar cases. Among these may also be included the develop- 
ment of tuberculosis after childbirth and abortions. Parkes-Weber 
also mentions massage as a possible etiological factor in reactivating 


Loe. cit. 
Miinchen. med. Wehnschr., 1899, 14, 346. 
Berl. klin. Wehnschr., 1914, 41, 246. 


on 


MEDICAL EXAMINATION FOR LIFE INSURANCE 643 


dormant tuberculous processes and producing acute progressive 
disease. 

Expert Testimony in Cases of Traumatic Tuberculosis. —Traumatic 
tuberculosis has of late been a cause for claims for damages and the 
physician testifying in such cases, irrespective whether he qualifies 
as an expert or not, must be prepared to discuss the following points: 
(1) Whether there is tuberculous disease in an active stage; (2) if so, 
has it been caused by the alleged injury; (3) in cases in which a pre- 
viously existing tuberculous lesion has been aggravated by an injury, 
it is important to bring out the manner in which such aggravation 
occurs; (4) the effects of the tuberculous process on the working capa- 
city of the plaintiff; (5) the outlook for a permanent cure; (6) the 
effects of the disease on the plaintiff’s social life. 

The first four points have been discussed in detail in the preceding 
pages. But it is important, when testifying for the plaintiff, to point 
out that even if curable, tuberculosis leaves a stigma on an individual 
living in a community in which the dangers of infection have been 
emphasized, and even exaggerated. Though it is entirely unjustified, 
people shun one with tuberculous disease, present or past, will not rent 
him a room in their homes; that it may interfere with his or her plans 
for marriage; that he is really a menace to infants whom he may infect 
by even slight contact, etc. It is also to be brought out that even after 
the disease is arrested, there is a possibility, in many cases, a probabil- 
ity, of a relapse which will disable him, or at least interfere with his 
working capacity. 


MEDICAL EXAMINATION FOR LIFE INSURANCE. 


It appears from statistics published by various life insurance com- 
panies that the losses sustained by these corporations paying death 
claims during the first few years of insurance are immense. Charles 
Lyman Greene! quotes a detailed report of one of the largest and 
most carefully conducted American Companies, which represents an 
analysis of 46,525 deaths constituting the total mortality from 1847 
to 1898 inclusive. Of these deaths no fewer than 5585, or about 12 
per cent of the total mortality, were charged to tuberculosis; 3307 
deaths occurring in policyholders during the age period of twenty to 
forty-five, while in the age period of twenty-five to thirty they repre- 
sented 32 per cent of the total mortality. No fewer than 594, or 18 
per cent of the former group, died during the first two years of insur- 
ance, 1769, or 53.5 per cent, during the first five years, and in the 
latter age period (between twenty-five and thirty) 10 per cent of deaths 
from tuberculosis occurred during the first year of insurance, and 30 
per cent during the first two years. 

Bearing in mind that the insured are a select class, having been 


+ Medical Examination for Life Insurance, Philadelphia, 1905, p. 198, 


644 MEDICO-LEGAL AND INSURANCE ASPECTS 


examined medically before acceptance, and all who show any of the 
stigma of disease are supposed to have been eliminated, the following 
figures are illuminating.’ They represent a comparison between the 
mortality rates from pulmonary tuberculosis in twenty-four Registra- 
tion States and the experience of the Industrial Department of the 
Metropolitan Life Insurance Company. 


Metropolitan 
Twenty-four Life Insurance 
Registration Company, 
States. Industrial. 
L914 |) 2) CU) See eR eee ee eee ee eee oS 185 
L915 ace, | ee ER ae cea) ad See eee ee meee OS 180 
LOVG: F602 Pre oe ih Re CR ee oe Lo, |! 173 
ARS Wy eee me ae) or Lope ewn Ae RP Nett ah Pe es le! alse 172 
LOIS: Fhe) ok A Mee. en ee Pe Pee ead 50) Abell 
1919 3c PTE A a a ee, ee 142 


It is clear that despite the attempts on the part of the medical 
departments of the insurance companies to weed out all who have 
tuberculous lesions, and also that a large number of deaths due to 
tuberculosis in insured persons are recorded as due to other causes, a 
fact well known to medical men, the loss sustained by these corpora- 
tions, and by fraternal organizations, is excessive. ‘There is no doubt 
that careful medical examination, by physicians qualified to do it, 
would materially reduce the number of deaths due to tuberculosis 
during the first three years of insurance and save millions to these 
companies and the policyholders. Of course, it cannot be expected 
that all be weeded out by medical examinations, because it is evident 
that policyholders are just as liable to develop tuberculosis as others. 
Careful medical examinations could also prevent the rejection of 
applicants for policies for alleged tuberculosis, or so-called predisposi- 
tion to the disease, without justification, as is observed daily in medical 
practice. In such cases an injustice is done to both, the insurance 
companies and the applicants, for obvious reasons. 

Elimination of Tuberculous Risks.— Obviously those who suffer from 
the active and progressive forms of the disease are rejected. In the 
advanced stages of the chronic forms of the disease this is clearly an 
easy matter for the medical examiner. In most cases the hectic flush, 
the emaciation, tachycardia, dyspnea, etc., are sufficient. In some 
instances, however, external appearances are deceptive; patients with 
large cavities in the lungs, with thick and adherent pleure, etc., may 
present a healthy countenance, and perhaps even be of normal weight, 
or over. In incipient cases, and they are liable to succumb sooner on 
the average than the just mentioned class, external appearances are 
of little, if any, value in estimating an insurance risk. 

In attempting to eliminate tuberculous individuals the examiner 
may be guided by the following points. 

The Family History.—It appears that the value of the family history 
in the diagnosis of tuberculosis has been overestimated. While the 


' Public Health Reports, 1921, 36, 1178, 


MEDICAL EXAMINATION FOR LIFE INSURANCE 645 


death rates of infants descended from tuberculous stock is very much 
higher than of others, adults of this class have not been shown to de- 
velop phthisis to a degree as to bar them from insurance. Familial 
tuberculosis affects mainly infants; the susceptible are weeded out 
during the first few years of life. Statistics carefully collated do not 
prove conclusively that descendants of tuberculous parents who sur- 
vive to adolescence are all doomed to end in phthisis. There is good 
evidence to the effect that when they do develop tuberculosis, the 
disease is likely to run an exceedingly chronic course, tending to 
recovery (see p. 621). Insurance companies have, however, found by 
experience that a family history of tuberculosis in the ascendency 
results in an excess of death claims. Rusher and Kenchington! investi- 
gated this problem among a group of 80,000 policyholders with a 
family history of tuberculosis, the total experience comprising 622,462 
policy years, and an average observation period for each policyholder 
of nearly eight years. They found that the mortality experienced in 
the early years of insurance was heavy, especially for young ages at 
entry. After the first five years of assurance the excess mortality is 
less marked, especially in the case of endowment policies, in which it 
comes well within normal limits. The latter fact suggests the impor- 
tance of “selection” by the insured; of the “bad life’ more or less 
consciously choosing a whole-life policy rather than an endowment. 
For these reasons, in addition to very careful examination, those with 
a family history of tuberculosis should be given rated policies when 
found otherwise acceptable. 

Past Diseases. —Signs of tuberculous disease during childhood, which 
are mainly seen as scars remaining after diseases of the glands, bones 
and joints, should not in themselves be taken as grounds for rejection. 
There are but few persons who had not been infected with tubercle. 
which has left traces in the intrathoracic glands, pleura and lungs. 
But these pathological changes are not perceptible to the average 
examiner. If those with scars on the neck are to be rejected efforts 
should be made to discover all who have sclerosed and calcified 
glands at the hilus of the lung for rejection, which is obviously not 
feasible nor rational. We have repeatedly shown that these glandular 
and osseous stigmata of past tuberculous disease are no signs of exces- 
sive predisposition to tuberculous disease in the adult; in fact, there is 
ample evidence of the effect that it is a sign of resistance higher than 
the average. The fact that it is exceedingly rare to find scars on the 
necks of patients with active tuberculous disease of the lungs, attests 
to this contention (see p. 586). Here again, when tuberculosis does 
develop in these persons, which is exceedingly rare, it usually runs a 
very chronic course, tending to recovery. However, these individuals 
are apt to develop acute miliary tuberculosis with implication of the 
meninges. Fifty per cent of cases of tuberculous meningitis in adults 


1 Jour. Institute of Actuaries, 1913; quoted from Tubercle, 1920, 1, 161. 


646 MEDICO-LEGAL AND INSURANCE ASPECTS 


have had extrathoracic tuberculous disease, especially of the genito- 
urinary tract, active, quiescent or healed. For this reason this class 
should not be accepted without reservation. Applicants with scars 
of the kind just mentioned, showing no signs of tuberculous disease 
of the lungs, who are well nourished and appear generally healthy, 
may be accepted on rated, or perhaps endowment policies. Straight 
whole-life policies should not be given to them. This suggestion is 
supported by the statistical evidence gathered by the American 
Medico-Actuarial Investigation of 1914 in which it is shown that 
in insured persons who gave a history of an attack of tuberculosis of 
bones (hip, ete.), there were 44 deaths as against an expected number 
of 23.14; the ratio being thus 190 per cent of the expected mortality. 
In insured persons whose history indicated an attack of bone tuber- 
culosis more than ten years before the application, the ratio was only 
120 per cent of the expected mortality. 

Pleurisy is most important in this connection. We have shown that 
an enormous proportion of those who recover from pleurisy develop 
pulmonary tuberculosis sooner or later (see p. 512). The statistics 
gathered by the Medico-Actuarial Investigation of 1914 showed that 
in insured persons giving a history of an attack of pleurisy within five 
years prior to the application, the death rates were about three times 
the normal; five to ten years prior to application, about twice the 
normal; and when the history indicated an attack over ten years before 
application for insurance, the death rate was about normal. For this 
reason, all applicants with a history of pleurisy should be rejected, at 
least within ten years following the attack of pleurisy. We have shown 
that most cases of tuberculosis following pleurisy occur within ten years 
after the acute disease, and that more than three-fifths of patients pass 
through life without developing phthisis. Moreover, a distinction is to be 
made between so-called primary, or “idiopathic” pleurisy, which is with 
but few exceptions tuberculous, and those accompanying pneumonia, 
especially influenzal pneumonia, which are not tuberculous. But the 
medical examiner who sees the applicant years after the attack of this 
disease can hardly make this fine distinction. Hence, applicants 
who have had pleurisy, but have been well for ten or more years, and 
on careful examination of the chest no signs of any active tuberculous 
process can be discovered, may be considered for rated policies. A 
history of pleurisy during childhood, and of empyema, is not to be 
considered as a load, or as predisposing to tuberculosis. 

Of other diseases, it is important to mention that influenza, which 
was formerly considered as predisposing to tuberculosis, has been found 
to have no influence on the subsequent development of this disease 
(see p. 128). If the patient has recovered and shows no signs of 
pulmonary changes in the lungs or pleura, the later evolution of tuber- 
culous disease will depend on factors other than the attack of influenza. 
Likewise, persons “subject to colds,” if these “colds’’ are not in them- 
selves indications of active tuberculosis of the lungs, which can be 


MEDICAL EXAMINATION FOR LIFE INSURANCE 647 


discovered by an examination of the chest, are no more predisposed to 
tuberculosis than others. Applicants “subject to colds’ should 
therefore be carefully examined; postponed in doubtful cases. If, on 
several examinations, spread over a period of six months or a year, the 
cough and expectoration are found to be undoubtedly due to rhino- 
pharyngeal changes, while in the lungs no pathological changes can be 
detected, tuberculosis should be disregarded within the same limits 
as In the average individual. 

A history of having been in a sanatorium for tuberculous patients 
should excite great diligence while examining the applicant, and 
caution before the issuance of a policy is recommended. It must, 
however, be borne in mind that sanatorium residence does not invari- 
ably prove that the patient has been tuberculous, or was so even at the 
time he lived at the institution. A large number of “suspects” are 
admitted, kept for months 1 in sanatoriums, and discharged as “non- 
tuberculous,” or as “ cured”’ of a disease which they never ay Many 
are discharged as “suspects.”’ We have already shown that 20 to 50 
per cent of sanatorium patients are sputum negative (see p. 584), 
and hardly 15 per cent of persistently sputum negative cases are sick 
with phthisis. The writer has seen many cases that were rejected by 
life insurance examiners merely because they had been in sanatoriums 
though they never had any conclusive symptoms or signs of tubercu- 
losis. A careful inquiry should be made in every sputum negative 
case as to the symptomatology before, and during residence at the 
institution, the course of the disease for which treatment was applied, 
and especially as to the sputum findings. If these point to a non- 
tuberculous condition, and there are no signs of any lung lesion, past 
or present, particularly if the applicant is examined more than five 
years after his residence at the sanatorium, he may be considered for 
a policy. Several postponements may be necessary in some cases. 
Outright rejection is unjust in many cases. 

On the other hand, those who had undoubted symptoms of tuber- 
culosis while at the sanatorium should be rejected. Elsewhere in this 
book are given statistical investigations by Elderton and Perry, Noel 
Bardswell, and others, on the mortality of patients after sanatorium 
treatment (see p. 726); they show that they are not good insurance 
risks. 

A history of hemoptysis, even without a distinct history of tuber- 
culous disease, while not invariably proving that the subject is likely 
to develop active phthisis, yet is sufficiently serious to excite caution 
on the part of the examiner. ‘The Medico-Actuarial Mortality Investi- 
gation found that policyholders with such a history gave the following 
mortality : 


A. One attack within five years of application chore as Sted tie 5 LOL 
B. One attack between five and ten years of woplisation” BP Pay ete OLS 
C. One or more attacks, the last more than ten years prior to application 102 


648 MEDICO-LEGAL AND INSURANCE ASPECTS 


In group A the death rates from tuberculosis were fully five times the 
normal. In group C they were nearly twice the normal. It is thus 
clear that a history of hemoptysis is a distinct load, and justifies 
rejection even if the physical signs elicited on the chest are not con- 
clusive of an active lesion. 

History of Exposure to Infection.—'This may be disregarded because 
there is hardly a resident in a large city, or a worker in any industrial 
or mercantile establishment brought into contact with many people, 
who has not met with tubercle bacilli “carriers.” If exposure to 
infection were a load, physicians would surely have a higher mortality 
rate from tuberculosis. It appears that when infected those who had 
not come into contact with tubercle bacilli carriers, are likely to con- 
tract acute and progressive tuberculous disease. Primitive people, 
brought into civilized countries, would make very poor risks for life 
insurance companies because of their liability to contract tuberculosis 
in its acute forms. Yet they were born and raised in an environment 
free from tubercle bacilli. Intimate exposure to infection has not been 
found effective in increasing the rate of morbidity and mortality from 
tuberculosis in adults. As was shown at length (see p. 149) conjugal 
tuberculosis 1s very rare. R6mer mentions that life insurance com- 
panies in Germany, basing their action on statistical experience, do not 
reject persons because of a history of exposure to infection, or who live 
with tuberculous consorts. George Florschiitz! in his work on insur- 
ance selection, says that “in medical selection one must certainly 
consider the risk of infection when it is so evident as in conjugal inter- 
course, but in general, as far as life insurance is concerned, one may 
regard tuberculous ‘infection as purely a matter of chance.’ He 
brings statistics showing that “of 1428 deaths from tuberculosis, there 
were but 11 in which the husband and wife of the deceased were 
tuberculous.” We have also shown that healthy workers in sana- 
toriums and hospitals for consumptives are no more liable to tuber- 
culous disease than others (see p. 147). The average adult living with 
a tuberculous individual in one house is hardly as much exposed to 
infection as are physicians, nurses, and orderlies in hospitals and 
sanatoriums. 

General Appearance.—In its relation to tuberculosis the weight of 
the applicant for a policy should be considered to a certain extent. 
Fat individuals only rarely develop phthisis. On the other hand, 
“fat phthisis,” though rare, does occur and, irrespective of the weight 
of the applicant, a careful examination of the chest is to be made. 
Persons under weight are to be carefully examined for physical signs 
of lung disease because phthisis is the most common cause of emacia- 
tion. Bisbee? found that those above the standard weight gave 5.59 
per cent of consumptive deaths; those with standard weight, 25.91 
per cent; those below standard weight, 42.51 per cent. These figures 


1 Medical Record, 1915, 87, 957. 
2 Quoted from Greene, loc. cit., p. 365. 


MEDICAL EXAMINATION FOR LIFE INSURANCE 649 


were based on 3548 cases. However, it is well known that many of the 
slim and wiry individuals live long. An applicant for a policy who is 
underweight, who shows no signs of present or past tuberculous changes 
in the lungs, and is incidentally free from sugar in the urine, or indica- 
tions of some other cachectic disease, may be passed in accordance with 
the rules of the company. In most cases in which loss of weight is a 
recent acquirement, and these are the ones that must be guarded 
against, there is a flabby skin, and caution is indicated. 

The following external signs should direct that attention of the 
medical examiner for Vigilante while examining the chest: A hectic 
flush; skin eruptions of the type of pityriasis versicolor, acnitis, folliclis 
(see p. 269), etc.; enlarged veins on the chest, especially unilaterally; 
clubbed fingers, inequality of the pupils, atrophy of the muscles of 
respiration, excavations above and below the clavicles and supraspinous 
fossee. Wherever any of these signs are noted on inspection in one 
who is underweight, the physical exploration of the chest must be 
thorough and systematic. 

Physical Exploration of the Chest.— No proper examination of the 
chest can be made unless the applicant’s clothing is entirely removed 
to the waist. Experts in physical diagnosis, and they are as rare 
among medical insurance examiners as among the profession in general, 
will frequently fail to detect a gross tuberculous lesion in any stage of 
the disease when the examination is made while the chest is covered. 
Incipient and limited lesions can hardly thus be detected and persons 
with incipient lesions only too often apply for life insurance. Raising 
the shirt is insufficient; it must be completely removed. As far as the 
writer’s observations have taught him, this is frequently not done. 

The appearance of the chest will give ample clues, if properly observed 
and interpreted. The flat chest in itself is no indication of active 
tuberculosis, as was already indicated (see p. 302), and it is decidedly 
wrong to refuse insurance to one merely because he has a narrow, flat 
and long chest, when no symptoms and signs of any tuberculous 
changes in the lungs can be elicited. To be sure, this form of chest is, 
in many cases, an indication of past tuberculosis, especially of the 
tracheobronchial glands. But we have shown that it points to healed 
tuberculous adenitis of the type most people pass through during child- 
hood. These persons are not tuberculous, and there seems to be avail- 
able evidence showing that they have been to a certain degree immu- 
nized against the graver and more acute forms of this disease. Acute 
progressive phthisis is most frequently seen in individuals with excellent 
and capacious chests, in athletes, pointing to lack of acquired immuniz- 
ing forces which protect the average individual. On the other hand, 
local retractions of the chest wall, atrophy of the respiratory muscles, 
etc., should be given careful attention. Scars indicating operations 
for empyema should not be considered of importance in themselves as 
indicating tuberculous lung disease, present or potential, because 
empyema, in adults as well as in children, is not a predisposing factor 


650 MEDICO-LEGAL AND INSURANCE ASPECTS 


to tuberculosis. Likewise, deformities of the chest, the result of 
rickets during infancy, the rachitic chest, are no indications of an 
excessive predisposition to tuberculosis. 

In looking for signs of tuberculosis most attention should be con- 
centrated on the region of the lungs above the third rib, the apices. 
With but few exceptions, rales, when heard unilaterally in these regions 
are indicative of tuberculous disease. No applicant should be recom- 
mended for a policy in whom rales are heard over the upper third of the 
chest anteriorly or posteriorly. It is immaterial what-kind of adven- 
titious sounds are heard exclusively in these regions, be they dry or 
moist, consonating, whistling, sonorous or sibilant, if they are heard 
over the apex, especially unilaterally, they offer sufficient ground for 
rejection. 

If tuberculosis is to be detected in its early stage, when applicants for 
insurance are apt to apply for admission, it is even more important to 
scrutinize carefully the breath sounds heard over the upper lobes of the 
lungs. We have already emphasized the fact that in really incipient 
lesions no rales may be heard at all but that in nearly all cases there 
are certain, though variable, changes in the character of the breath 
sounds (see p. 339). The following hints may prove of assistance in 
efforts to eliminate tuberculous risks: If the breath sounds are weak, 
feeble, or absent in one of the apices, there is ground for caution. 
Urging the applicant to cough may provoke rales, or crepitation, in 
the same area. In others, the expiratory murmur may be prolonged, 
or bronchial in character; in some bronchovesicular breath sounds are 
heard. If the resonance over the apex is impaired over the area with 
feeble breath sounds tuberculosis is to be thought of. It is well to bear 
in mind that these changes are usually heard in early cases over the 
“alarm zone’ (see p. 379). Also that changes in breath sounds 
limited to a circumscribed area, are more important in this regard than 
when heard all over the chest. 

It is, however, unfair to reject an applicant for insurance merely 
because of some slight changes in the breath sounds and resonance of 
the chest, even when found over the apices, especially the right apex. 
In many cases this is one of the anomalous physiological phenomena 
consistent with perfect health and longevity; or it may be an indication 
of some pathological process in the lung or pleura which has never 
given trouble and healed perfectly. In such cases it is urgent that 
certain other features of the applicant should be inquired into before a 
decision is arrived at. 

Constitutional Symptoms.—The most important effect of active 
tuberculosis is the production of toxic symptoms. Without symptoms 
of toxemia active tuberculosis is rare. These can best be determined 
by a study of the constitutional symptoms of the case as outlined in 
other parts of this book. It is clear that the insurance examiner is 
not in a position to make a careful clinical study of the applicant. 
Moreover, at the time he submits to an examination the applicant may 


MEDICAL EXAMINATION FOR LIFE INSURANCE 651 


be afebrile, though if carefully studied, it would be found that he runs 
one of the various types of fever already described as characteristic of 
tuberculosis in the incipient stage (see p. 217). 

But there is one symptom of tuberculous toxemia which is only 
rarely lacking and cannot be concealed. Tachycardia is one of the 
cardinal symptoms of active tuberculosis; bradycardia is extremely 
rare; even a normal pulse rate is very uncommon. Hence, if there are 
some doubtful physical signs detected in the chest, and the pulse rate is 
rapid, the applicant is to be rejected. If nervous influences are 
suspected as the cause of acceleration of the pulse, postponement is in 
order. This is a point which, if followed, would prevent many medical 
examiners from passing tuberculous applicants for insurance; it would 
also prevent the rejection of healthy persons because of some slight 
alterations in the resonance and breath sounds of the chest. When the 
rate of the pulse is around normal, 70 or less per minute, and the appli- 
cant appears well nourished, slight alterations in the breath sounds 
may be disregarded. At any rate, the applicant may be postponed 
for three to six months, and if there are no changes in the physical 
signs, and especially if the nutrition of the patient is well maintained, 
he may be recommended for a policy, provided the examiner is satisfied 
that during the period of postponement the applicant continued at his 
occupation. If he has been away for a rest, this may be detected in 
many cases by noting the parts of the skin which are exposed to the 
action of the sun rays, the hands, shoulders, face, ete. As a rule, a 
vacation leaves unmistakable traces on these parts. 

Following the above diagnostic principles might save the insurance 
companies millions which are annually paid out for deaths which occur 
during the first two or three years of insurance. It would also prevent 
the rejection of many applicants for insurance because of “ tuberculosis” 
which is subsequently shown to have been non-existent. 


CHAP E Rik tee 


INDICATIONS FOR TREATMENT OF PHTHISIS. 


THE indications for treatment in pulmonary tuberculosis appear at 
first sight to be simple and clearly defined. On the principle that the 
first thing to do is to remove the cause, it would seem that there are 
but two procedures to follow: To destroy the bacilli which have 
settled within the body; or to increase the resisting powers of the 
patient, and thus render the soil unsuitable for the growth of the 
invading virus. But in this case, the ideal, like other ideals, cannot 
be achieved in the average case, and the aim at curing the patient by 
the first of these procedures is not feasible at the present state of our 
knowledge. 

We have no chemical remedy which will destroy the bacilli harbored 
within the body without simultaneously killing the patient. We have 
no drug which will render the tubercle bacilli harmless in the body, 
as quinin destroys the malarial parasite, or arsphenamine and 
mercury destroy the spirocheta in syphilis, leaving the patient in good 
shape. Even the so-called specific treatment—the various tuberculins, 
sera, and vaccines—which have been lauded for their alleged curative 
powers when properly administered, are not stated to have any known 
bactericidal action, nor are they known to hinder the proliferation of 
the bacilli within the body, or to immunize the tissues against the 
poisons engendered by these microdrganisms through the production 
of antibodies, as is the case with antitoxins. Attempts at active 
and passive immunization have not met with notable success in 
tuberculosis. 

The etiology of tuberculosis, however, teaches a lesson in rational 
therapeutics. The tubercle bacilli do not grow with equal facility in 
every individual; if they did, the number of human beings who suc- 
cumb to this disease would be equivalent to the number that give posi- 
tive reactions to tuberculin, indicating that they have been infected 
with tubercle bacilli—over 90 per cent of the adult population in 
large urban centers. We have seen that the bacilli can proliferate and 
produce their noxious effects only in persons who offer a favorable 
soil for their existence. 

In what this favorable soil consists, we are not altogether clear. 
In the chapters on Phthisiogenesis we discussed it in detail, and it was 
evident that everything which undermines the general health of a 
person and reduces his vitality may prepare a favorable soil for the 
growth of tubercle bacilli within the body, and thus produce phthisis. 


POLYMORPHISM ON THERAPEUTIC INDICATIONS 653 


As a corollary we may argue that anything which will stimulate the 
vital defensive forces, which are more or less inherent in every indi- 
vidual, or which will improve the nutrition of the body may hinder 
the proliferation of the bacilli, and with the improvement in the gen- 
eral physical condition of the patient the local lesion may cicatrize, 
or the dissemination of the bacilli by metastasis may be prevented. 

This is what modern phthisiotherapy is aiming at in handling each 
individual ease of the disease. As has been pointed out by G. 
Schréder,! modern therapeutic tendencies, which are based on the 
achievements of immuniology, have not changed our methods of treat- 
ment of tuberculosis, especially phthisis. It is today, as it has been 
hitherto, based on the general principles of therapeutics, because 
phthisis as a disease cannot be considered an infectious disease swt 
generis. It can only originate in individuals with a certain constitu- 
tional susceptibility, which may be inherited or acquired. 

Air, Food, and Rest.—The traditional therapeutic triad—air, food, 
and rest—has withstood the test of time, and is at present called into 
service more often than ever before in the treatment of phthisis. 
Indeed, like many other excellent therapeutic agents which have 
become standard, it is very often abused. Many patients know of it 
and quite often tell their doctor that they are aware of the fact that 
medicine is helpless and that air, food, and rest are all that they need. 
Curious to say, some physicians do not protest. 

But this is all wrong. The medical man of today has many more 
resources in his attempts at curing phthisis and should not rely on 
the above-mentioned triad exclusively. Indeed, a physician who 
advises a patient to lead an open-air life in some region famous for its 
beneficial effects on this disease, and urges him to consume more and 
better nourishment than he has been in the habit of taking, and to 
stop all life activities, fulfills but part of his duty to his patient. There 
are many more therapeutic resources which hasten recovery, relieve 
the most annoying and painful symptoms of the disease, and go a 
long way toward prevention of complications, which cannot be met by 
the above-mentioned indications. 

Effects of Polymorphism of the Disease on Therapeutic Indications. 
—Since the etiological unity of tuberculosis has been proved by the 
discovery of the tubercle bacillus, the profession has tacitly accepted 
that unity of origin invariably implies unity of effect, and the treat- 
ment of the disease was also unified. But this is an error. We have 
seen that the tubercle bacilli produce different lesions in different 
individuals, as regards the anatomical changes in the lung, the clinical 
phenomena, and the course and curability of the disease. Indeed, 
there are hardly two cases of phthisis which appear exactly alike on 
the autopsy table, and all the groupings into caseous, fibroid, cavitary, 
pneumonic, ete., are inadequate. This is especially true of the clinical 


1 Handbuch der Tuberkulose, 1914, 2, 1. 


654 INDICATIONS FOR TREATMENT OF PHTHISIS 


manifestations of the disease; its polymorphism is noteworthy and 
important. To be sure, this is also true of other diseases, notably 
syphilis, yet the specific remedies in the latter answer most of the 
indications: So long as we are not in possession of a specific remedy 
or tuberculosis, it will have to be treated symptomatically. 

Under the circumstances, to be effective, treatment must be applied 
in accordance with the clinical manifestations encountered, and to a 
certain extent with the clinical form of the disease. We have seen that 
each form pursues a course more or less different from all other forms. 
It would therefore be wrong to treat a patient with abortive tubercu- 
losis in the same manner, and for the same length of time, as one with 
chronic progressive phthisis. Fibroid phthisis demands different treat- 
ment from chronic caseous phthisis; febrile cases cannot be treated 
like those which run an afebrile course. The various complications 
of the disease, like intestinal, laryngeal, and renal tuberculosis, demand 
special care which the general indications do not satisfy. Preéxisting 
disease, like syphilis, diabetes, cardiovascular and renal derange- 
ments, etc., alter the course of treatment appreciably. There are also 
differences in our methods of treatment when we care for a tuberculous 
child, as compared with those applied in adults; but in senile phthisis 
the indications are not the same as those in adolescents. The indica- 
tions are even different in cases of young, single women, as compared 
with married or pregnant women, and during the menopause tuber- 
culosis often demands special treatment. 

It is thus obvious that a method of treatment which will suit all 
cases cannot be formulated. What may be efficacious in one may not 
be feasible in another, or even harmful in a third. The treatment of 
phthisis must be individualized to suit the case; it must be elastic and 
adaptable to the polymorphous nature of the disease and to the various 
accidents and complications occurring during its course. 

Criteria of Efficacy of Treatment.—In judging the value of any 
method of treatment, we must bear in mind some points which are 
usually neglected while speaking of this subject. The fact must not 
escape us that the vast majority of cases of tuberculosis manifest a strong 
tendency to recover under any method of treatment, or even spontaneously. 
Impressed by the malignancy of the disease in many cases, we are apt 
to forget the large number of spontaneous recoveries, and when we 
meet with good results, we are likely to attribute them to the method of 
treatment pursued, forgetting that a large proportion of patients would 
have recovered without the treatment. 

Discussing the clinical features of abortive tuberculosis, we have 
shown that this form of phthisis is very common and may not be 
recognized. When reading about a large proportion of recoveries in a 
sanatorium which admits only “incipient” cases, or of a drug which is 
alleged to cure at this stage a certain proportion of cases, etc., we must 
recall that among these “early” cases, there are a large number with 
a strong tendency to recovery under all circumstances. To be of real 


CRITERIA OF EFFICACY OF TREATMENT 655 


value, a method of treatment must be effective in producing more recoveries 
than would be ordinarily anticipated. 

Even in the forms of chronic phthisis which usually last for many 
months or years before terminating in recovery or death, the course Is 
not always progressive, continuously advancing. This is evident from 
the large number of patients who give a history of hemoptysis, cough, 
fever, emaciation, pleurisy, etc., five, ten, or more years before the onset 
of the present illness, which was diagnosticated at the time as tubercu- 
losis, but the patient did well. For long years he had been able to 
attend to his work, only being laid up now and then for a few days with 
an attack of “bronchitis,” “grippe,”’ ete., but this last attack has 
proved persistent. Now, if in this case a proper diagnosis had been 
made during any of the previous attacks, the prompt recovery would 
have been credited to the special treatment applied. In fact, many 
patients tell us that a certain prescription was very effective for years 
in relieving them promptly, but this time it has failed. 

All properly investigated statistical examinations have shown con- 
clusively that five years after the onset of active phthisis about 50 
per cent of the patients are in good or fair physical condition and 
even able to make themselves useful at their respective occupations 
irrespective of what method of treatment was applied. The statistics 
of results obtained in sanatoriums show that patients discharged in 
the advanced stages of the disease are often found alive and active, 
five, ten, or even fifteen years later. A physician who keeps careful 
records and publishes a series of cases in which such results are shown 
can impress the profession that his method of treatment has done 
wonders. Yet it is just what should be expected under any harmless 
method. 

A study of the literature on phthisiotherapy shows that nearly all 
authors, urging their methods, report certain and almost the same 
percentages of patients “cured,” “disease arrested,” “improved,” 
“unimproved,” and last, but always least, “dead.” Practically all 
sanatoriums, whether located on high or low altitudes, at the sea- 
coast or inland, in cold, warm, or moderate climates; irrespective of 
the special method of treatment pursued—indoors, outdoors, or in 
tents; no matter what the fad or hobby of the attending physician, be 
it dietetic, medicinal, or specific; they all give the same results if we 
should judge them by the percentages of reported cures, improvements 
and deaths as published in their annual reports. 

During the first year or two after the introduction of new drugs or 
specifies, physicians report excellent results, as is seen from the litera- 
ture on creosote and arsenic and their derivatives, ichthyol, cinnamic 
acid, iodin, tannin, succinimide of mercury, ete. They all cured a 
certain percentage, arrested the disease in a larger percentage and 
failed only in very acute, progressive, or far-advanced cases. Phthisio- 
therapy has thus been encumbered with an enormous number of 
medicaments which have been lauded by many competent and con- 


656 INDICATIONS FOR TREATMENT OF PHTHISIS 


scientious physicians at one time or another, and condemned with 
equal vigor by others. According to Rénon the popularity of each drug 
or method of treatment hardly exceeds three years. 

These are, in fact, the reasons why so many new methods of treat- 
ment, drugs, specifics, climates, diets, etc., are annually announced as 
curative agents for tuberculosis. They all depend on the normal pro- 
portion of recoveries which occur under any method. That charming 
French writer, Louis Rénon,! says in this connection: “All new thera- 
peutic methods of treatment of tuberculosis, so long as they are harm- 
less, always give the same satisfactory results. This is an axiom which 
I should like to have printed with heavy type in all the new books on 
phthisiotherapy. It is an axiom which may be clinically translated 
into this simple statement: Hurry and take the treatment as long 
as it cures: if you wait you may be too late.”’ 

The reasons for these therapeutic illusions are found in the above- 
stated facts. The disease is acutely progressive in comparatively few 
cases. In these, all agree that their remedies are of no avail and they 
are not counted in the reported cases. In a large proportion there is 
a strong tendency to spontaneous cure, and they furnish the recoveries 
for the special climates, specific and empiric therapeutic agents, for 
the “milk cure,” the “song cure,” the “grape cure,” ete. In the 
majority of cases of active phthisis the disease runs an undulating 
course, with more or less frequent exacerbations of acute or subacute 
symptoms, followed by remissions in the activity of the process. In 
some the acute exacerbations are very infrequent, long remissions are 
obtained, the patient feeling comparatively well for several months 
and the credit is given to the method of treatment. 

Psychic Influences.— Persons under the influence of mild alcoholic 
intoxication are very susceptible to suggestion, and the consumptive 
who is under the influence of tuberculous toxemia is very vulnerable 
to auto and heterosuggestion, as was shown in Chapter XIII. Any 
new drug, especially when boosted in the newspapers, Is apt to relieve 
him ina remarkable manner. We often meet with consumptives who 
keep on sinking while under the care of a physician, but for some 
reason are impelled to change their medical adviser and, though the 
latter makes no changes in the treatment, the patient begins to gain 
in health and general well-being. This is usually the result of a new, 
careful, and minute physical examination by some pedantic physician 
who subjects his patient to all the diagnostic procedures—inspection, 
palpation, percussion, and auscultation; “gives him the benefit of the 
latest of diagnostic aids,” the v-rays, the cutaneous or subcutaneous 
tuberculin test, examines the sputum and urine in the presence of the 
patient, etc., and usually gives the same directions as those of the 
former physician, but more minutely; orders the patient to report 
frequently to see whether any changes are necessary. This is often 





1 Le traitement pratique de la tuberculose pulmonaire, Paris, 1908, p. 30. 


SUGGESTION BY TUBERCULIN TREATMENT 657 


the beginning of a most remarkable improvement in a case that has 
been going from bad to worse: The appetite returns, the cough ceases, 
the nightsweats disappear, etc., and he gains in weight and strength. 

Suggestion by Tuberculin Treatment.—There are many phthisio- 
therapists, competent to give authoritative opinion, who are convinced 
that tuberculin, as generally administered in minute doses, acts more by 
suggestion than by specific action on the tuberculous process in the 
lung. We shall revert to this subject while speaking of specific treat- 
ment. But meanwhile we want to point out the powers of suggestion 
in specific treatment as shown in a drastic manner by Albert Mathieu 
and Dobrovici,! who announced to the tuberculous patients at the 
Andral Hospital in Paris that a new discovery had been made, a 
new serum had arrived for the cure of tuberculosis, and that shortly 
a sufficient quantity of the remedy would be available for those in need 
of it. The patients had to wait for some time, and when the*serum 
arrived they all rejoiced. The new remedy consisted simply of physio- 
logical salt solution, but was given the pompous name Antiphymose. 
Certain patients were told that they were fit subjects for antiphymose, 
while others were denied the treatment on the plea that it would not 
do them any good. ‘The selected patients were placed under careful 
observation and their histories were again recorded minutely, so that 
all felt that they had been seriously given the first opportunity to 
benefit by a great discovery. No change was made in the surroundings 
of the patients and the diet, but all other medication was discontinued. 

The patients were greatly impressed by the new remedy and the 
favorable results exceeded all expectations. Within a couple of days 
there was noted an improvement in the appetite; those who had fever 
before showed a normal temperature, and the cough, expectora- 
tion and nightsweats were ameliorated; those who had hemorrhages 
ceased bleeding, and even the physical findings in the chest showed dis- 
tinct signs of amelioration of the process. The gain in weight was 
remarkable, ranging from 1500 gms. to 2 and 3 kilos. As soon as the 
injections were discontinued all the old symptoms reappeared. 

From personal experience? with the culture of turtle bacilli injected 
by Dr. F. F. Friedmann into patients under my care at the Monte- 
fiore Hospital in New York City, I can say that its effects were practi- 
cally the same as those of Mathieu’s antiphymose. The heightened 
susceptibility to suggestion of the average consumptive was _ here 
vividly illustrated. No one will deny that the vast majority of people, 
healthy and sick, are amenable to suggestion in various ways, but it 
must be acknowledged that a group of patients suffering from acute 
or subacute gout or rheumatism, heart disease in a state of decom- 
pensation, of nephritis complicated by dyspnea and dropsy, of ulcer 
of the stomach, of cancer, or of any other organic pathological entity, 


1 Bull. gén. de therapeut., 1908, 151, 882. 
2 Fishberg: Interstate Med. Jour., 1914, 21, 349. 
42 


658 THE INDICATIONS FOR TREATMENT OF PHTHISIS 


would not be influenced to the same extent by suggestion as were the 
consumptives just mentioned. 

It appears that consumptives in all stages of the disease are sus- 
ceptible to psychotherapy. I have repeatedly observed marked 
improvement in the subjective symptoms of patients who were told 
by their physicians that nothing could be done for them because they 
are doomed, while the new physician, who was promptly called because 
of the extreme prostration of the patients, assured the unfortunate 
sufferers that there was no danger at all, and that only careful treat- 
ment was necessary to rehabilitate the lost health and strength, and 
afterward a short visit to the country would enhance the chances for 
ultimate recovery. I have seen improvement in a patient after three 
punctures were made in her chest with a view of inducing an artificial 
pneumothorax, but no nitrogen was introduced into the pleura because 
of adhesions. Yet the temperature, which had been quite above nor- 
mal for weeks, promptly dropped to normal and the patient felt well. 
That tuberculous patients, as a rule, improve during the first few 
weeks or months in a new resort or institution is a well-known fact; and 
that it is usually not the superior climatic conditions or the different 
method of treatment that is efficacious in this respect is proved by 
their relapse into their former condition, or by the aggravation of their 
disease, after the novelty of the new surroundings begins to wear off. 
This is the main reason why climates “wear out.” 

Psychotherapy in Tuberculosis.—This heightened susceptibility of 
the tuberculous patients to suggestion is of immense value and assist- 
ance to the physician who is the fortunate possessor of a personality 
which stands him in good stead when handling difficult and intract- 
able cases. But it is a double-edged sword. It also interferes in a 
large measure with the proper appreciation of the value of any thera- 
peutic procedure, because the patients are apt to be impressed with 
any new remedy, especially if it has been puffed up by an enthusiastic 
physician, and promptly improve. But the improvement is only 
short-lived, and within a short time all the old symptoms return, as 
we have shown. 

This psychic trait of the tuberculous is, however, of immense value 
in assisting physicians in their efforts to alleviate the more painful 
features of the disease, provided they know how to take advantage 
of it. Indeed, the success of many physicians in handling tuberculous 
patients depends on this point, and it is a fact that therapeutic nihilists 
fail, as a rule, to give relief to this class of patients. The detailed, 
often written, instructions given by physicians to their patients in 
sanatoriums, the minute doses of tuberculin administered, the vigilant 
anticipation of reactions, and the careful inquiry as to the effect on 
the constitutional symptoms, have all the elements of suggestive thera- 
peutics. Without these details, institutional treatment of tubercu- 
losis, especially in private and costly sanatoriums, would be a failure. 

For these reasons medicinal treatment of tuberculosis has a place 


THE INDICATIONS FOR TREATMENT 659 


in the therapeutics of tuberculosis. The materia medica is of 
assistance not only in alleviating certain annoying symptoms, as we 
will show later on, but rational medication also imbues the patient 
with the idea that something is being done for him during his long and 
trying disease. Medicinal preparations are palliative, to be sure, 
but they often carry the patient over an acute crisis with more or 
less comfort which could not be obtained otherwise, and they stimulate 
a hopeful outlook for an ultimate recovery. 

The Indications for Treatment.—In the absence of specific remedies 
the therapeutic aims are to increase the natural forces of resistance of 
the tissues by constitutional treatment and by direct local treatment 
of the affected lung. The first indication is met by certain general 
therapeutic measures, the second by the induction of an artificial 
pneumothorax. In this book the treatment of phthisis is discussed 
with a view of methodically presenting the subject in the following 
order: 

. Prophylactic treatment. 
. General management of the case. 
. Dietetic management of the case. 
. Institutional treatment. 
. Climatic treatment. 
. Medicinal treatment. 
. Specific treatment. 

8. Symptomatic treatment. 

9. Local treatment. 
10. Treatment of the various forms of tuberculosis. 
11. ‘Treatment of the complications. 


“ID OF De 


GHAR TEREX XoGhy: 
PROPHYLAXIS. 


Tue recent discoveries in the field of phthisiogenesis have shown 
that the prophylaxis of tuberculosis is much more complex than the 
simple formule or programs of antituberculosis societies would indi- 

cate. A considerable part of the sure preventives given in popular 
and technical literature have been shown to be inefficacious or super- 
fluous by the newer teachings of the bacteriology, immunology, demog- 
raphy, and the clinical phenomena of this disease. 

Modern prophylactic measures should differ in accordance with 
what we aim at attaining. If our aim is to prevent infection with 
tubercle bacilli, we must take different measures from those which are 
indicated when we aim at preventing phthisis, the disease caused by 
these microdrganisms. In our attempts at preventing tuberculosis in 
children we must resort to other prophylactic methods than when 
we aim at preventing tuberculous disease in adults. In fact, measures 
which are likely to prove effective in infants are not indicated in older 
children, while in adults most of the measures which have been found 
effective in early life are futile, extravagant, and even harmful. 

Prevention of Infection.—We have seen that the child is born free 
from tuberculosis, even if its parents are tuberculous at the time of 
conception or birth. We have also seen that during the first year of 
life some become infected and that the proportion showing signs of 
harboring tubercle bacilli in their bodies keeps on gradually increasing 
with advancing years so that at ten years the vast majority are infected, 
and that at the age of fourteen over 90 per cent react to tuberculin— 
an unmistakable sign of having been infected with tubercle bacilli. 

We have also shown that during the first year of life infection, if it 
does occur, is likely to result in an acute or subacute disease which 
proves fatal in nearly all cases. On the other hand, after passing the 
age of infancy infection becomes less dangerous, only rarely causing 
death, though it is liable, when localizing itself in glands, bones, and 
joints, to cause prolonged sickness and end in disfigurement, if the 
patient survives. 

Our main aim is therefore clear. The infant under two years of age 
must be protected against tuberculous infection at all costs. In 
families in which there is no tuberculous member this is a simple 
matter. Impressing the parents that infants acquire tuberculosis 
very readily, as easily as measles, scarlet fever, influenza, etc., and 
that a single exposure is liable to result in infection, they can, with 
reasonable and ordinary care, shelter their young offspring against 
the tubercle bacilli. Especially is this an easy matter with mothers 


PREVENTION OF INFECTION 661 


who suckle their babies, and do not give them any cows’ milk, so that 
bovine infection is entirely excluded. 

An infant is naturally not apt to come in contact w ith strangers 
unless those who care for it bring it in their proximity. Realizing that 
there are so many persons with open tuberculosis who are considered 
quite healthy, or who consider themselves healthy, “carriers” in the 
full sense of the word, it is obvious that in order to positively avoid 
infection at that age, infants must not be brought in contact with any 
one excepting the immediate family who are known to be free from the 
disease. 

But it must be remembered that the immediate family includes the 
grandparents, and they are often suffering from latent tuberculosis. 
The impression is gaining ground of late ‘that a large proportion of 
the chronic bronchitis, pulmonary emphysema, osthmes ete., in aged 
persons, is of a tuberculous character, as was already show n in the 
chapter on Phthisis in the Aged. The writer in attempting to trace 
the source of infection has often found that it was the coughing or 
expectorating grandfather or grandmother who was seca for 
the disease in an infant. 

Great care is to be exercised in selecting domestic servants for homes 
with infants. Especial care is to be taken with the nurse for an infant. 
She should be carefully examined by a physician, and reéxamined if 
she acquires a “cold” that lasts more than a week. 

These simple measures suffice in homes in which there are no tuber- 
culous inhabitants. No infant should be allowed to remain in a home 
in which a phthisical person resides. Even if the patient is one of the 
most scrupulous, and takes excellent care of his sputum, he should not 
live in the same home in which an infant is raised. This is a point 
which, in our efforts to prevent the dissemination of the disease, is 
often overlooked. Following up phthisical patients, the authorities 
usually state that a careful consumptive is harmless, so long as he 
takes care of his expectoration, and permit tuberculous persons to 
live in the same home with infants. But as a matter of fact the harm- 
lessness of consumptives extends only to adults, and not because they 
are taking extreme care of their expectoration, but for other reasons 
which will be given later on in this chapter. As regards infants, no 
care, however conscientiously exercised, can surely prevent infection. 
And infection in infants is likely to prove deadly. 

The indications are therefore clear. Either the phthisical person 
or the infant is to be removed. No compromise can be allowed in 
such cases. 

No tuberculous mother is to be allowed to rear her young children, 
especially during infancy. It has been found that very few infants 
survive when suckled by a mother suffering from phthisis. ‘The 
extensive statistics of Weinberg,! embracing 5000 families with 18,000 


1 Die Kinder der Tuberkulésen, Leipzic, 1913. 


662 PROPHYLAXIS 


children, have shown that the nearer the birth of the children to the 
time of death of their tuberculous parents, the higher the mortality 
among them. Three-fourths of the children born during the last 
year of life of tuberculous mothers succumb; and 90 per cent of the 
children born during the last month of life of tuberculous mothers die. 
The investigations of the present writer! among children of tuberculous 
parentage in New York City have shown practically the same condition 
to prevail. In addition to the excessive mortality in general, 16 per 
cent of the deaths among children under six years of age were due to 
tuberculous meningitis, as against only 1.27 per cent among the 
general population of New York City. 

The prophylactic value of separation of the infant from its tuber- 
culous parents is well exemplified by experiences with tuberculous 
animals. Harlow Brooks? shows that in cattle the question of whether 
or not the offspring becomes tuberculous depends entirely upon 
exposure after birth. It has been conclusively shown that the calves 
are very rarely, if ever, infected before birth, but that the slightest 
carelessness in exposure of the newborn calves to infections leads to 
certain disaster. It has been found that tuberculous animals may be 
utilized for breeding purposes and that they may be crossed and inbred 
with entire disregard of the factor of tuberculosis and purely for the 
purpose of improving or maintaining the type, provided the calves are 
separated from the parents immediately after birth. 

Similar measures have to be taken in cases of newborn infants of 
tuberculous parentage. If the mother is tuberculous the infant is 
to be removed immediately after delivery, and should not be allowed 
in her proximity during the first two years of life. If the father is 
phthisical, he should be removed from the home so long as there 
are infants under two years of age. In some cases the alternative of 
removing the infant may be more feasible. Bernheim induced 
three tuberculous mothers who had twins to separate with one child 
each, while retaining the others in their homes, though healthy wet- 
nurses were employed to suckle the babies. The three isolated children 
remained healthy, while the three which were raised at home suc- 
cumbed to tuberculosis. Armand-Dellile studied a series of 787 
children born or living in 175 families one or more members of which 
were tuberculous. Of these children 323 were placed in the country 
and all did well; 396 were not removed from their tuberculous environ- 
ment, and of these 328 developed tuberculosis. Figures like these 
show how imperative it is to separate infants from their tuberculous 
parents more drastically than any other evidence. 

Available evidence tends to show that the infant is not infected 
through ingestion of the milk from its tuberculous mother, but through 
the bacilli she eliminates while speaking or coughing. Human milk 
is only rarely found to contain tubercle bacilli, so long as there is no 


1 Archives of Pediatrics, 1914, 31, 96, 197. 
2 Am. Jour. Med. Sci., 1914, 148, 718. 


PREVENTION OF INFECTION 663 


tuberculous disease of the breasts. Stanley L. Wang! and Frederick 
Coonley examined the breast milk of 28 tuberculous women; specimens 
from 15 cases were injected intraperitoneally into guinea-pigs. In 
all cases the results were negative, no tuberculous changes being 
found in the animals at the autopsy; 450 microscopic examinations of 
specimens of milk were taken bi-weekly from the whole series of 28 
cases. ‘These were all negative, excepting 1, which was positive once, 
and | other specimen from the same case, which was suspicious once. 
A.B. Marfan? reports similar experiences. He says that tubercle bacilli 
have only exceptionally been found in human milk. A few experiments 
have produced tuberculosis in animals after injecting them with milk 
taken from the breasts of tuberculous women. There are but two 
authentic reports of infants being infected by the milk of their mothers. 
These were the cases of Demme and Roger and Garnier. 

It is noteworthy that improvement in the sanitary and hygienic 
conditions, which are so effective in preventing phthisis in the adult, 
as will be shown later on, are not of any value in the case of infants. 
As has been pointed out by Romer, it was found that scrupulous atten- 
tion to hygiene and sanitation of the stable, such as proper construc- 
tion, ventilation, cleanliness, etc., hardly has any influence on the 
prevalence of tuberculosis in cattle, and that only strict isolation of 
the sick from the healthy animals is effective. Primary infection in 
infants appears to follow the same law: Exposure of an infant, even 
in an ideal home, may result in fatal tuberculosis, while life under 
adverse conditions will not produce tuberculous disease, unless there 
is a source of infection, which is usually the human consumptive and 
rarely milk derived from tuberculous cows. In the development of 
phthisis in adults hygienic and sanitary conditions play, however, a 
very important role. 

The prevention of bovine tuberculosis is not to be neglected. When 
an infant must be hand fed, the milk should be carefully selected. In 
large cities the only drawback is the cost. Certified milk is every- 
where available, but it is rather expensive and prohibitive for the vast 
majority of the population. For this reason all milk that is not derived 
from a source known to be safe is to be pasteurized or, better yet, 
sterilized. Pasteurization does not always destroy all tubercle bacilli, 
as was shown by Hess. On the other hand, an investigation by E. C. 
Fleischner and Kk. F. Meyer,’ in San Francisco, showed that in certified 
milk bovine tubercle bacilli were not present in sufficient number to 
infect guinea-pigs. Certified milk is thus the safest for infants. How- 
ever, the main problem is the human bacillus, as was already shown. 

These simple measures are to be taken with a view of successfully 
preventing primary infection of infants under three years of age. 
They can be easily carried out by any family that has some degree 


1 Jour. Am. Med. Assn., 1917, 69, 531. 
2 Le nourisson, 1916, 4, 34. 
3 Am. Jour. Dis. Children, 1917, 14, 157. 


664 PROPHYLAXIS 


of economic independence. In families which are to some extent ham- 
pered because of economic stress, the State is to interfere. Health 
Boards, which are busy protecting adults against infection to which 
they are hardly susceptible, could perform really useful service if they 
concentrated more and more along these lines. The mortality during 
the tender age of infancy, which has hardly been influenced by the 
‘ampaign against tuberculosis, would be reduced to a minimum. 
Moreover, massive infection, which is apparently responsible for 
phthisis in adults who have survived it during infancy, may thus 
be largely prevented. 

Prophylaxis in Children Over Three Years of Age.— When the child 
begins to walk around and comes in contact with many people, pre- 
vention of infection is not simple. The parents, especially those who 
cannot afford a maid for each child—and they constitute the bulk of the 
population—lose control over their children, unless they are prepared 
to keep them altogether from contact with strangers, and this is not 
feasible for obvious reasons. Later when they go to school, they are 
bound to come in contact with other children and adults, and it is 
altogether impossible to prevent their meeting tuberculous individuals, 
no matter what the economic condition of the parents. It is thus clear 
that it is quite if not altogether impossible to prevent tuberculous 
infection among children over four or five years of age. 

But, as was shown in Chapter XXIV, infection in children over four 
years of age is usually relatively harmless. Either no disease at all 
occurs or rarely tracheobronchial adenopathy results, which is serious 
only in exceedingly rare instances. 

Available evidence tends to show that in infants infection is usually 
accomplished within the family—tuberculosis is exceedingly rare in 
infants who live in homes in which there is no phthisical member. 
When this is the case, we may trace the infection to someone living 
in the house as a lodger, or to some relative or friend who visits the 
home and comes in intimate contact with the infant, thus causing 
massive infection. “It is said that after two infant children of a royal 
house had died of miliary tuberculosis it was discovered that their old 
nurse had a tuberculous infection of the maxillary sinus with a fistulous 
opening into the mouth through which mucus laden with tubercle 
bacilli frequently passed.’ (Bushnell.') With children of play and 
school age, the opportunities for intimate contact with adult strangers 
are scarce; they are not taken in the arms, not kissed indiscriminately, 
etc., and even when infection takes place, it is from another child, a 
playmate, etc., is slight, and not so massive as it is likely to be in infants, 
who are infected from adults. 

There is abundant clinical evidence of the relative harmlessness of 
infection of children over four years of age. One has but to consult 
the mortality returns in any country to convince himself that between 


1 Wpidemiology of Tuberculosis, New York, 1920, p. 177. 


PREVENTION IN CHILDREN 665 


three and fifteen years of age the mortality rates from tuberculosis 
are comparatively low, despite the fact that over 90 per cent of the 
tuberculous infection of humanity takes place during this period of 
life. Comparing the results of infection during the first two years of 
life, and those taking place between four and fifteen years of age, the 
contrast is striking and convincing (see p. 453). Neither acute tuber- 
culosis nor chronic phthisis of the adult is common in children of 
school age. Thus, among 925,000 children examined by the medical 
school inspectors in New York City during the school year September, 
1914 to June, 1915, only 68 were found tuberculous.’ When we bear 
in mind that each was examined by physicians and nurses once in six 
weeks on the average, and that a complete physical examination was 
made of all children three times during the course of the elementary 
school year, and that a cough noted by the teacher was sufficient to 
refer the child for examination, it is obvious that not many suffering 
from tuberculosis were overlooked. 

Under the circumstances, we may conclude that no matter what 
the cause is, infection of children during school age is comparatively 
harmless, and that, inasmuch as experience has taught that everybody 
is bound to be infected with tubercle bacilli, the best that can happen 
is that infection should occur at the age period of four to fourteen 
years. The primary mild infection at that age, as we have shown 
above, practically vaccinates humanity against more severe infections 
in later years. Otherwise, all adults would be as susceptible to tuber- 
culous disease as are guinea-pigs or the indigenous races of Central 
Africa. 

Our efforts are therefore to be directed, next to the prevention of 
contact of infants with tuberculous persons, at the prevention of 
massive infection of children. This can be done within certain limits 
by preventing children from associating with individuals suffering 
from open tuberculosis. The danger lurks mostly in adults, because 
children expectorating tubercle bacilli are exceedingly rare. 

Prevention of Reinfection.—It thus appears that the bacilli infecting 
children remain dormant within the body and cause no disease so 
long as there are no predisposing or exciting causes. We know that 
under certain circumstances these dormant bacilli activate and cause 
disease by metastatic auto-infection. This is mainly seen in cases in 
which, owing to defective nutrition, or some intercurrent disease, 
notably measles, whooping-cough, typhoid, ete., the resistance is 
reduced, and an exacerbation of the tuberculous process takes place. 
Moreover, it appears that the younger the child, the more is the anergy 
thus induced likely to be followed by active tuberculous disease. The 
indications are therefore clear—young children and infants are to be 
sheltered against the endemic diseases. Special care is to be exercised 
in this direction with children of tuberculous parentage, who have in 





1 Weekly Bulletin of the Department of Health, City of New York, 1915, 4, 289. 


666 PROPHYLAXIS 


all probability suffered from massive infection. This class of infants 
is to be scrupulously shielded against measles, whooping-cough, scarlet 
fever, diphtheria, ete. If these diseases are bound to attack them, it 
is best that it should occur after they have passed the fourth year 
of life. 

During convalescence after any of these endemic diseases, the child 
is to be given special care with a view of prevention of metastatic 
auto-infection while the body is in a state of anergy; in other words, 
susceptible to tuberculous infection. This may be accomplished by 
either taking the child to the country, preferably the seashore, for a 
few weeks or months, till it has completely recuperated; or, when it 
must be kept at home, it should be given proper nourishment, and kept 
outdoors the greater part of the day, and it should sleep in a room with 
open windows. 

Artificial Immunization.—We have emphasized that tuberculous 
infection confers a certain degree of immunity against reinfection with 
the same virus (see Chapter V). It is this immunity of the tuberculous 
to tuberculosis that has suggested attempts to procure artificial im- 
munity by vaccination with living tubercle bacilli. ‘The most impor- 
tant work along these lines was done by Behring, who vaccinated cattle 
with human bacilli to which they have shown a certain degree of 
resistance. Romer did the same with sheep, and more recently F. F. 
Friedmann announced that he has succeeded in immunizing children 
against tuberculous disease by inoculating them with an emulsion of 
living turtle bacilli. 

So far the results of animal experimentation along these lines have 
not been encouraging. It appears from Behring’ s and Roémer’s 
pr ophy lactic inoculations that immunity was not attained in all cases, 
and in the few that it was, the resistance to infection was rather short- 
lived, lasting but a few months. Friedmann’s claim that tuberculous 
disease is prevented by his turtle bacilli vaccine has been found un- 
founded. Itis clear that the vaccinated children will have to be watched 
for at least thirty years before agreeing that they are immune to 
pulmonary tuberculosis. During childhood this disease is quite rare 
(see p. 453). 

More recently, Calmette and Guerin’ reported remarkable results 
attained by prophylactic inoculation of cattle with attenuated bovine 
bacilli. The fatty capsule which envelops the tubercle bacillus has 
been found to consist of an alcohol which is not unlike cholesterol. Bile 
salts are capable of dissolving, or at least holding in colloidal suspension, 
certain lipoids as cholesterol. Inasmuch as the difficulty encountered 
in attempts at destroving tubercle bacilli is due to their fatty capsules, 
bile is thought to be capable of rendering this capsule vulnerable. 
On this principle Calmette believes he attained attenuation of the 
tubercle bacilli by cultivating them for twelve years, through seventy 


1 Annales de l’Inst. Pasteur, Paris, 1920, 34, 553; L’infection Bacillaire et la Tubercu- 
lose, Paris, 1920, p. 577. 


PROPHYLAXIS IN ADULTS 667 


transfers on glycerolated potato treated with bile. However, the few 
animals (cattle) which Calmette reports as having been immunized 
by the vaccine of these attenuated bacilli, are not sufficient encourage- 
ment to proceed with similar vaccination of human beings. 

In general it may be stated that prophylactic vaccination has not as 
yet given encouraging results. 

Prophylaxis in Adults.— Prophylaxis in adults is no more a problem 
of infection. It may be taken for granted that everyone who has passed 
through the first fifteen years of life, especially in a city, has been 
infected with tubercle bacilli. The fact that he shows no symptoms 
and signs of disease is no proof that he has escaped infection, as was 
already shown. In adults, the problem is the prevention of disease, 
of phthisis. I believe that a considerable portion of the inefficacy of 
the campaign against tuberculosis is due to the lack of appreciation 
of this distinction between infection and disease. 

This fact is based on the newer investigations in phthisiogenesis, 
which have conclusively proved two points: 

1. That chronic phthisis in the adult, of the type that creates most 
of the tuberculosis problem, never occurs immediately after a primary 
infection; if disease occurs at all soon after a primary infection, it Is 
of the acute types of tuberculosis of the lungs or of other organs. 
Indeed, when disease follows immediately after a primary infection 
of an adult it is almost invariably deadly, as is seen in tuberculosis 
of primitive peoples who had not been exposed to infection during 
childhood. 

2. Infection with tubercle bacilli, whether it causes disease or not, 
renders the body immune against further and renewed exogenic infec- 
tion with the same virus. Inasmuch as nearly all adults have been 
infected with tubercle bacilli during their childhood, they are immune 
against reinfection with bacilli which may be eliminated by tuber- 
culous persons. The phthisical manifestations in adults are attributed 
to infection during childhood, just as the tertiary manifestations 
of syphilis are late results of the original infection years ago, though 
the body is immune against renewed exogenic infection with the same 
virus. 

If this were not a fact, practically all the workers in hospitals for 
consumptives would succumb to the disease: all consorts of tuberculous 
persons would acquire the disease. One has to consider that of women 
married to, and living with, husbands suffering from active syphilis, 
hardly any escape infection. But we see thousands of tuberculous 
persons living with consorts, having children with them, yet the 
unaffected consorts remain in good health, as we have already shown 
in detail (see p. 149). 

It is therefore a vain effort to follow up tuberculous persons, push 
them from pillar to post, interfere with their employment, as has been 
done in many cases, with a view of preventing infection of fellow- 
workmen. If these individuals cannot infect their husbands or wives, 


668 PROPHYLAXIS 


as the case may be, despite the intimate contact, they are surely not 
a menace to their fellow-workmen. 

This fact is now beginning to be recognized by those who are well- 
informed about the recent progress in our knowledge of phthisiogenesis. 
There has been manifesting itself a reaction against the absurd and 
cruel phthisiophobia w hich has been rampant for about twenty-five 
years. Baldwin! says: “Adults are very little endangered by close 
contact with open tuberculosis, and not at all in ordinary association. 

It is time for a reaction against the extreme ideas of infec- 
tion now prevailing. There has been too much read into the popular 
literature by health boards and lectures that has no sound basis in 
facts and it needs to be dropped out and revised.”’ 

We have shown that while the mortality from tuberculosis has 
decreased during the past few generations, infection of human beings 
has gone on to a degree as could never have been higher. There are 
sagacious physicians who believe that it is fortunate for humanity 
that infection has not completely been conquered. ‘‘ We have done our 
best during the last quarter century to diminish tuberculous infection,” 
says Bushnell,? “and something has been accomplished, no doubt, in 
lessening the size and frequency of infecting doses. Fortunately as 
yet we have not succeeded in diminishing by one iota the morbidity 
of the disease. Not that such diminution, and that to the point of 
extinction, is not desirable, but we are not yet ready for it. For as 
soon as we diminish the morbidity the danger arises that the oppor- 
tunities for tuberculization will likewise diminish, and after a deceptive 
lull cases of acutely fatal tuberculosis will begin to take the place of the 
former more benign types of the disease.” 

Prevention of Phthisis.—It appears that in the eager ohne after the 
bacteria, which could never be entirely destroyed, we have forgotten 
that only a small portion of those infected develop phthisis, while 
the rest are apparently benefited by the infection. Some recent 
writers have not hesitated to apply the term benevolent infection to 
those who have been fortunate in acquiring tuberculosis during later 
childhood and have thus been immunized against primary infection 
after fifteen years of age, when the disease produced by a primary 
infection is apt to run an acute and fatal course. Otherwise, we 
would all succumb to the acute and fatal forms of tuberculosis. 

Phthisis is a disease occurring in persons who have been infected 
with tubercle bacilli many years before the outbreak of the disease. 
It is due to reinfection. But available evidence appears to point in 
the direction that the reinfection occurs from within, that it is metas- 
tatic; the bacteria which have remained dormant for years are slowly 
or suddenly reawakened into activity, and they produce new lesions; 
and that exogenous reinfection is exceedingly rare, if at all possible. 

We know that certain conditions favor a reduction in the normal 


1 Johns Hopkins Hosp. Bull., 1913, 24, 220. 
2" Loc. cit., p. 1&3; 


PHTHISIOPHOBIA 669 


resisting powers of the body and permit the proliferation of the dor- 
mant bacilli. Among these, inferior sanitary, hygienic, and economic 
conditions stand out preéminently. We have seen that the rates of 
wages, the number of rooms in which a family lives, the character 
of the work pursued by an individual, ete., have a strong influence in 
the direction of enhancing or preventing the evolution of phthisis. For 
this reason, the philanthropic agencies may do more toward the 
prevention of phthisis by concentrating their attention on improve- 
ments along economic lines of reform than by sending agents to tell 
adults ae it is danger ous to remain in the proximity of a consump- 
tive. Labor unions do better by exacting higher wages and shorter 
hours than driving unfortunate phthisical persons from their places of 
employment, as is being done of late in New York City. 

Phthisiophobia.—Phthisis is undoubtedly an exacerbation of dor- 
mant tuberculous processes in the lungs; its entire clinical course is 
undulating, with periods of quiescence -interrupted by periods of 
activity. These acute and subacute exacerbations may be prevented 
by careful attention to the general health of any individual who shows 
the least tendency to phthisical disease. Such individuals should not 
be hounded, refused employment, etc. They are to be helped along in 
the direction of securing easy work during the quiescent periods, so 
that they may be self-supporting and pole nce The words of 
an intelligent and observing consumptive on this subject are to be 
borne in mind by social w orkers, who of late seem to know more of the 
etiology and prevention of tuberculosis than those who have made ¢ 
special study of the subject. Says the American historian, William 
Garrot Brown, in his Confessions of a Consumptive: 

“The public depends for protection from such danger as our con- 
tinued existence involves, not on its own exertions but on ours. To 
render that protection we must burden ourselves with both expense 
and trouble. We must incessantly take, for the sake of the public, 
precautions which are disagreeable and costly; and meanwhile a great 
part of the public is, by its attitude toward us, steadily tempting us, 
and even sometimes fairly compelling us, if we would live to discon- 
tinue these precautions and go on as if there were nothing the matter 
with us. The folly and stupidity of this attitude it is impossible to 
overstate. It is of itself by far the chief cause and source of the per- 
sistence of this scourge. 

“Ixnown and recognized and decently entreated, we are not dan- 
gerous. Shunned and proscribed and forced to concealments we are 
dangerous. Victims ourselves of this same régime of ignorant and self- 
deceiving inhumanity, we are called on every hour of our lives for a 
magnanimous consideration of others. Society can hardly find it 
surprising or a grievance if our human nature should sometimes weaken 
under the strain of the incessant provocation it endures from this 
strange working of human nature in general. Why should we alone 
be expected to be guiltless, always to our own cost and sacrifice, of 


670 PROPHYLAXIS 


that very form of man’s inhumanity to man from which we ourselves 
are suffering more than anybody else? Yet I can honestly attest that 
the vast majority of us are guiltless of any merely resentful offense; 
that, as a rule, when we fail to protect the public it is only because 
the public compels us to disregard its interest, its safety. This is what 
I earnestly entreat the public, for its own sake, candidly to consider. 

‘“Candidly means fully. If the public is to be safe from us, if the 
public is to continue to have our protection from that against which 
it failed to protect us, then the public must make it possible for us 
to get—it must certainly cease to make it impossible for the mass 
of us to get anything except by subterfuge—what we must have to 
live. Weare neither criminals nor mendicants. We do not ask favors, 
we merely revolt against a mean and stupid oppression. We revolt 
against ignorance and against a lie. The public would get rid of us, 
and thereby makes us inescapable. It would pretend, and would have 
us pretend, that we are nowhere. It thereby insures that we shall 
be everywhere. It proscribes us and thereby admits us.” 

If the average consumptive was not shunned by adults; if he was 
permitted to work unmolested after he is cured or the disease is arrested, 
or quiescent, allowing him to earn his livelihood, a considerable part of 
the economic stress caused by this disease would be done away with. 
If the tuberculous individual is told that he is only a menace to infants, 
less dangerous to children, and not at all dangerous to adults, he will 
surely take all precautions against infecting those who may be harmed 
by it. 

But at present the State, municipal, philanthropic and social agencies 
that send out representatives telling those who live with consumptives 
that the patients must be shunned, and incidentally conveying the 
information that a careful patient, 7. e., one who takes care of his 
sputum, is not at all dangerous, even to infants. Some patients in New 
York City are actually dreading lest their names will be reported 
to the authorities, and they will be pestered by those well-meaning 
nurses, physicians, social workers, etc. Instead of telling the patient 
that he is only a menace to infants, and that he must keep away from 
them, they often visit his place of employment and the result is that 
the unfortunate patient is soon without a job and starving. 

The results of these methods of phthisiophobia are seen in the 
fact that the number of infants which succumb to tuberculosis has 
not decreased even in Germany where antituberculosis agencies have 
been most active; that the number of persons infected with tubercle 
bacilli has not decreased is clear when we consider that over 90 per cent 
of humanity react to tuberculin. 

I do not want to be understood as speaking unfavorably of all pro- 
phylactic measures against tuberculous infection of adults. There are 
many, especially among the richer classes in cities, and in suburban 
and rural districts, who have escaped infection during childhood, and 
they should be protected. It is, in fact, well known that tuberculosis 
when occurring in these classes is often of an acute type, just as it is 


DISPOSAL OF THE SPUTUM 671 


in the indigenous races of Central Africa or in the Esquimaux. They 
should be protected against the sputum indiscriminately expectorated 
by consumptives, and against droplet infection when coming in con- 
tact with persons suffering from active phthisis. But with the city- 
bred people, especially those who have survived in the congested parts 
of cities or the slums, there is hardly any danger that adults will be 
infected with tubercle bacilli. They have been infected during child- 
hood; vaccinated and immunized against additional infection. But 
it is just among these that the strong efforts are made to prevent 
exposure of adults to infection. The irony is that their infants are 
usually neglected by the social forces working in the antituberculosis 
campaign. 

Just as cattle breeders have found that the control of tuberculosis 
is mainly a matter of prevention of infection of newborn calves, and 
that adult cattle may be disregarded, so must we act with humans. 
To prevent infection, newborn infants must be protected while children 
over ten and adults need no special measures, especially those who 
have been raised in cities. 

Disposal of the Sputum.—In our attempts at preventing infection, 
the disposal of the sputum expectorated by phthisical patients is more 
important than any other prophylactic measure. The pathogenic 
bacilli are distributed in a virulent form only from one animal body to 
another. Exceptionally, the source of the bacilli is a domestic animal, 
mainly milk from tuberculous cows, but in the vast majority of cases 
the source of infection is sputum expectorated by phthisical patients. 

For this reason the rigorous laws prohibiting indiscriminate expec- 
toration which enlightened communities have inaugurated are fully 
justified, and they ought to be more rigorously enforced. It should be 
made clear that tuberculosis is not the only disease which is trans- 
mitted by expectoration, but many other diseases may be thus trans- 
mitted, so that nobody ought to spit on the floor of a house or public 
place. Furthermore, there are many tubercle bacillus “carriers” 
who do not suffer from the disease which they are liable to transmit, 
especially to infants and children. The fact that indiscriminate expec- 
toration is prohibited irrespective of the question whether the offender 
is tuberculous or not, makes it easier to exact it from the phthisical 
patients, who do not like to be stigmatized. 

In the case of children, especially infants, it is not only sputum which 
is dangerous, but also the droplets flying out of the mouth and nose 
during the acts of coughing, sneezing, and talking. For this reason a 
consumptive should not associate with infants, even if he is careful 
with his expectoration. Droplet infection may prove disastrous to 
infants. In the case of adults, coughing and sneezing are hardly dan- 
gerous. We have already mentioned Saugman’s conclusion that it 
is not dangerous for adults to be coughed at by a tuberculous patient 
(see p. 149). 

Cuspidors.—The disposal of the expectoration is therefore an impor- 
tant problem, and it has been suggested that the best means of render- 


672 PROPHYLAXIS 


ing it harmless is that it should invariably be deposited in some form of 
cuspidor. 

Floor cuspidors in rooms, especially in public places, are a nuisance; 
they cannot be tolerated in any decent home for both sanitary and 
esthetic reasons. ‘They are unsightly, and just as much of the sputum 
is often deposited around the vessel as within it. Flies, cats, and dogs 
are frequent visitors, and with mouths or legs covered with sputum may 
proceed further in their quest for food, and deposit the bacilli on food 
which is subsequently used by the inhabitants of the house. The 
elevated cuspidors, of which we find such beautiful illustrations in a 
certain variety of books on tuberculosis, may be good for certain 
institutions, especially those harboring advanced consumptives, but 
they should not be, and are not, used in homes and public buildings. 
They are also an invitation to spit; they provoke expectoration in 
persons who otherwise would not do it. This is the reason why they 
are hardly seen anywhere, except in books and institutions. 

The pocket sputum flasks are objectionable for other reasons. ‘Their 
variety is great, if we are to judge by the large number illustrated in 
popular books on the prevention of tuberculosis. The ingenuity of 
the designers or inventors is noteworthy and could have been used 
to better advantage in other directions. They are, however, not used 
outside of institutions to any noticeable extent. I fancy that a per- 
son who would take out a sputum flask, even one of those which 
look like cigar boxes, lunch boxes, etc., and spit into it within the 
sight of people in a public place, would create a miniature panic 
among some who have read popular literature on the prevention of 
tuberculosis. 

They are objectionable for another reason. No matter how wide- 
necked they are made, the patient must apply his lips to the mouth 
of the flask if he wants to deposit the sputum within it. The result 
is that part of the sputum sticks to the lips or mustache and beard, 
and this must be removed with a handkerchief. Even if all male 
patients would consent to shave clean it would not help. I have 
observed that the lips are very often covered with sputum after the 
patient has expectorated into any of these flasks. 

In institutions they should be used, and the ones made of pasteboard, 
kept in a tin frame-holder, are the best. Patients in the advanced 
stages of the disease should use them at home in case they expectorate 
large quantities of sputum. 

But I can see no reason for urging them on patients in the incipient 
stages of the disease, expectorating but little sputum. Physicians 
trying to imitate legislators who pass laws which they know cannot 
be enforced, defeat their own ends. We cannot induce a patient to 
carry a sputum flask with him, no matter how fine and deceptive its 
construction may be, and to use it in public. I have also known some 
patients in the incipient stages of the disease who left sanatoriums 
because they could not tolerate their fellow-sufferers walking around 


DUTIES OF COMMUNITY IN PREVENTION OF PHTHISIS 673 


with sputum cups in their hands. Advanced patients are hardened 
in this respect, as a rule. 

Patients in the incipient or quiescent stages of the disease can 
empty their chests in the morning into cuspidors containing some 
cheap disinfectant. It should soon be emptied into the water-closet. 
Urging them to burn it is usually a vain effort, if only because there 
are no facilities in modern homes for the purpose. Those expectorating 
considerable quantities may efficiently dispose of their sputum by the 
use of paper napkins. Toilet paper will also answer the purpose. 
Several thicknesses are folded once, so as to receive the sputum; the 
paper is again folded and the ends folded over so as to enclose the 
expectorated material, and then placed in a grocer’s bag (about 6 by 
12 inches). The bag can be pinned to the side of the bed, or clamped 
to the small bed-table. Several times a day, depending on the amount 
of sputum, the bag and its contents should be burned, if there are facili- 
ties for the purpose. The folded paper pockets containing the sputum 
may, however, be disposed of by dropping them singly into the water- 
closet and flushing it immediately. 

There is no question that there are valid objections to the handker- 
chief, though it is not so strong a menace as some writers would lead us 
to believe. But the average patient will use nothing else for reasons 
already stated. Portable sputum cups are used only in institutions 
and in homes, but, despite the agitation in their favor, we fail to meet 
persons in the streets or public places of any large city in the world, 
carrying and expectorating into them, although we know that thousands 
of consumptives are everywhere. Even if it is a compromise, we 
must submit to the inevitable and permit patients to use handker- 
chiefs. It is best that they should be made of gauze or cheap cotton, 
which may be destroyed after use; or they may be of Japan paper, 
which may be deposited into the water-closet which is immediately 
flushed. If made of better material, the handkerchief should be boiled 
before washing. Boiling is a better and surer bactericide, especially 
of tubercle bacilli in sputum, than any chemical disinfectant. 

Duties of the Community in the Prevention of Phthisis.—In its 
demands on the consumptive to shape his life in such a manner as to 
prevent the dissemination of the disease, the community must not 
neglect its own duties to the unfortunate individual, who is suffering 
to a great extent because of conditions which the authorities have 
permitted to prevail. The community must not only provide shelter, 
proper nourishment and medical attendance for those patients who are 
not in a position to procure it at their own expense, but must also see 
to it that the conditions favoring the development of phthisis should 
be eliminated. 

Laws regulating the sanitary and hygienic conditions of dwellings 
for the working people, among whom the proportion of phthisical 
patients is high, should be passed and rigorously enforced. ‘Tenement 
house laws, passed and enforced, have a greater influence on the reduc- 
tion of the morbidity and mortality from consumption than all the 

43 


674 PROPHYLAXIS 


lectures delivered in and out of season to social workers, policemen, 
teachers, and workmen, on the perils of the tubercle bacilli and the 
best means of killing them. The demolition of the old-style tenements 
with numerous rooms without windows has saved many more per- 
sons from developing phthisis than all the sanatortums which are 
supposed to isolate the sources of infection, but which, in fact, exclude 
those in the advanced stages and permit them to come into intimate 
contact with infants and children. The abolition of the sweat-shops 
in New York City deserves more credit for the prevention of phthisis 
than all the leaflets which have been distributed by so many over- 
lapping agencies, each eager to get at the persons who cough as a 
result of tuberculosis or some other disease and “follow them up.” 

Light and well-ventilated dwellings and workshops are of prime 
importance in preventing phthisis, and the community in which there 
are no rooms without windows and no sweat-shops or factories which 
are dark and badly ventilated has the least consumptives to care for. 

Good wages and short hours, allowing good nourishment, and time 
for outdoor exercises and recreation, are important in the control of 
phthisis. 

Marriage of the Tuberculous.—The problem of marriage is one 
which the physician often has to solve for his patients. We frequently 
have to answer the question whether a non-phthisical consort should 
continue to live with the phthisical partner; or whether a tuberculous 
patient, in any stage of the disease, may enter the married state. 
Answering these questions involves a consideration of several factors: 
The dangers of transmission of the disease to the non-phthisical con- 
sort; the dangers to the potential offspring; and the effect of the 
married state on the patient. 

The dangers of transmission of the disease to the consort are negli- 
gible. We have brought statistics proving that the unaffected consorts 
of consumptives are no more liable to become phthisical than others of 
the same age and social condition (see p. 149). The unaffected consort 
has undoubtedly been infected during childhood, and reinfection is not 
likely. Whether he or she will develop phthisis depends on factors 
other than intimate association with a tuberculous consort. The 
conclusion is therefore justified that, as regards transmission of the 
disease alone, there is no more danger in marriage of phthisical patients 
than in cases of cancerous or diabetic patients. Our answer is to be 
about the same as when two persons who had both been previously 
infected with syphilis ask whether they are permitted to marry.! 

1 In this connection it is interesting to cite the following lines from Metchnikoff: 
“At the age of twenty-three,’ he says, ‘I married a young lady of the same age who 
was attacked by grave pulmonary tuberculosis. Her condition of feebleness was such 
that it was necessary to carry her in a chair in order to mount the few steps which led 
to the church where our marriage was to be celebrated. . . . My wife died of tuber- 
culosis after four years of suffering. I passed the greater part of that time by her side 
in the greatest intimacy without taking any precaution against the contagion; never- 
theless, in spite of these conditions, which were especially favorable for catching the 


disease, I have remained free from tuberculosis, and that during forty-four years since 
my marriage.’’ (Bedrock, January, 1913.) 


MARRIAGE OF THE TUBERCULOUS 675 


The danger to the children that may result from the union is 
enormous. If the newborn child will remain in the proximity of the 
phthisical parent, it will most likely become infected during infancy 
and succumb. Under the circumstances, unless they are satisfied to 
remove the child immediately after birth and not see it till it has passed 
the first two years of life, phthisical patients should not procreate. 
This is a point which cannot be emphasized too strongly to tuberculous 
patients who are married, or contemplate marriage. It is especially 
dangerous for an actively phthisical woman to raise infants. They 
will, we can say almost without exception, acquire the disease and 
succumb during the first year of life. 

The effects of the married state on the patient are different in men, 
as compared with women. On the average male patient in the incipient 
or moderately advanced stages of the disease, sexual intercourse has 
the same effect as on the average person who is not in perfect health. 
If he indulges moderately, it does him no harm at all; in fact, it may be 
beneficial because it prevents brooding over enforced abstinence which 
is often seen among all classes of men. It also precludes venereal 
complications which may have an effect on the phthisical process. 

With women, things are different. So long as they do not become 
pregnant there are no strong and valid reasons against married life. 
In fact, among the working classes the married consumptive woman is 
better situated than the single who soon after becoming tuberculous 
also becomes a dependent; and if she has no family to care for her, 
she is doomed. The dangers of pregnancy have been overestimated 
by many authors, as we have already shown (see p. 579). It is clear 
that women with active and progressive tuberculosis are in grave 
danger after becoming pregnant; this has also been observed to be 
true of experimental tuberculosis in animals. But the intensely 
chronic, quiescent, and arrested cases are hardly ever harmed by 
marriage and pregnancy. ‘To be sure, it will be observed that a certain 
number, about 20 per cent, will suffer recrudescence of the disease dur- 
ing pregnancy and lactation, but taking a similar number of unmarried 
tuberculous women with quiescent or arrested lung lesions, we will 
have about as many reactivations during any two years which involve 
pregnancy and lactation. We have already given details as to the 
clinical criteria which may guide us while advising patients on these 
points (see p. 580). 

Married women with active tuberculosis are to be given detailed 
instruction on the proper methods of prevention of conception. If 
they become pregnant the induction of abortion is indicated and justi- 
fied both for the sake of the prospective child, which is bound to 
become tuberculous unless removed from the proximity of the mother 
immediately after birth, and for the sake of the mother, who is liable 
to succumb to acute or subacute tuberculosis soon after childbirth. 

The demands made by some enthusiastic advocates of eugenics that 
tuberculous persons should be prohibited by law from marrying, has 


676 PROPHYLAXIS 


no scientific basis in view of what has been stated above. The race 
is not in danger of deterioration because of children derived from 
tuberculous stock. We have already mentioned that tuberculous 
cattle have been used for breeding purposes by removing the calves 
immediately after birth. We see no reason why this should not hold 
in human beings. Moreover, prohibition of legal marriage does not 
exclude extramarital sexual intercourse and childbirth with their 
concomitants. Free instruction on the means of prevention of con- 
ception is more likely to eliminate phthisical stock, and thus prove of 
eugenic value, than prohibition of marriage. 

On eugenic grounds it has also been stated that tuberculosis is rather 
a benefactor of humanity. It removes the weakly, the decrepit; in 
short, the unfit. In time, it is thus argued, all the susceptible will thus 
be removed and the race will improve. But we have seen that it is not 
only the weakly and decrepit which are likely to be attacked. The 
large number of athletic youths who develop tuberculosis in the prime 
of life prove that the strong suffer as often as the weak; the enormous 
number of intellectual giants who have succumbed to tuberculosis 
(see p. 297) show that humanity would be the gainer by eradicating 
this disease. 

A patient presenting himself or herself with the problem of mar- 
riage should be explained the situation along the lines just detailed, 
and if he or she is intelligent, we may rest assured that the action will 
be reasonable for both the married people and the community. The 
ignorant and reckless will not consult us in such matters, and if they 
do, they will not follow instructions. For this reason, they should be 
left out of consideration in discussions of this kind. One thing I always 
insist on with my patients: The unaffected partner must be informed 
about the true state of affairs and given the choice. Very often it 
will be found that a good woman will greatly help along a consumptive 
toward recovery which could not have been attained if the patient 
had remained single; or that a female patient will recover after marriage 
to a man who gives her a good home, proper food, ete. 


CHAPTER XXXV. 
GENERAL MANAGEMENT OF THE CASE. 


Should the Patient be Told that He is Tuberculous?—The diagnosis 
of pulmonary tuberculosis having been definitely made, there arises 
the question whether the patient should be told the true nature of his 
disease. Many physicians are inclined to keep him in ignorance as 
to the true state of affairs, and to tell him that he is merely affected 
with a “mild bronchial catarrh,” “pleurisy,” a “‘protracted cold,” 
etc. Very often a patient is brought to the office by relatives and 
friends who beg the physician that in case tuberculosis is diagnosti- 
cated, the patient should under no circumstances be told the truth. 

There are many valid reasons against such a procedure. From the 
standpoint of the physician’s personal interest, it is bad practice. It 
is always to be borne in mind that the patient will, sooner or later, 
find out the truth and blame his doctor for deception, or more often, 
accuse him of ignorance and claim, with considerable justice, that had 
he been informed in time he might have taken better care of himself. 

But there are reasons of more importance than the doctor’s interest 
for tellmg the truth to every patient on such occasions. It must never 
be lost sight of that tuberculosis is transmissible, particularly to 
infants and children, and that the patient must be warned against 
the possibility of disseminating the seeds of the disease. This can 
only be done by telling the patient the true state of affairs, and giving 
him details of the principles of prevention. Moreover, the average 
patient knows that, in many cases, the chances of recovery diminish 
with the advance of the disease, and negligence in informing him of 
his opportunities at the earliest possible time may prove disastrous. 
We do not know of any quick cures, and the codperation of the patient 
is absolutely essential. He can only take proper care of himself and 
those around him when he knows the true situation. 

It is noteworthy that relatives and friends who have requested a 
physician to keep the patient in ignorance of the fact that he is tuber- 
culous are always grateful in the end when he is tactfully informed of 
the truth. 

Irrespective of requests of friends and relatives, the patient is to, 
be told plainly and unequivocally that he suffers from tuberculosis. 
In really incipient cases this can be done in several instalments, because 
it usually requires several examinations to make a positive diagnosis. 
When finally told, it is to be emphasized that he is in the incipient 
and curable stage, and assurances given that in his case the prognosis 


678 GENERAL MANAGEMENT OF THE CASE 


is very favorable. But it must be insisted upon that the patient’s 
coéperation is absolutely essential to attain a cure. An intelligent 
patient may be given details of the nature of the disease and it may 
be pointed out that his own determination to follow instructions is of 
more importance than all the medicines and climates; in fact, with- 
out his own coédperation, he is lost even if he consults the best known 
specialists, enters the most famous sanatorium, or emigrates to any 
climatic resort. It isa striking fact that nervous and excitable patients 
who are expected by their relatives to break down on hearing the 
truth, resign themselves to their fate and often display courage and 
determination worthy of heroes. 

“Unless we carry conviction to our patients,” says Arthur Latham,! 
“they are unlikely to put up with the restrictions which are inevitable 
to proper treatment. It is a disastrous thing to talk about a “weak 
spot” in the lung. It is our duty, in an overwhelming proportion of 
cases, to state his position frankly to the patient, to explain intel- 
ligibly the reasons for the treatment prescribed, and the possible pen- 
alties which may have to be faced if our advice is neglected. If we 
can convince our patient, we shall in all probability have won his 
loyal codperation, which is half the battle; if we fail to convince him 
or get him to see the reasonableness of our advice, we cannot expect to 
find treatment carried out with sufficient earnestness and consistence 
to be of real value.”’ 

The suggestion has been made by Penzoldt? that the dose of truth 
given to the patient should be in inverse ratio to the seriousness of 
the case—the less the chances of recovery the smaller the dose of 
truth. In incipient and hopeful cases the whole truth is best, but 
the term “consumption” should be avoided in all cases; “ tuberculosis”’ 
is a term which covers everything for the patient, though as we have 
seen, it is not exactly correct scientifically or clinically. But in the 
popular mind it has been of late considered a hopeful and curable 
disease, if taken in time. Some patients may be told that when 
neglected, “tuberculosis” may turn into consumption. 

It is different with advanced and hopeless cases. They present 
themselves asking whether their cough is really due to consumption 
and it is at times a pity to tell the unfortunate patients the true state 
of affairs; not unless we are not averse to shortening their days. Still, 
for obvious reasons it is always imperative that some relative or 
friend should be told the truth. Similarly, in cases of acute or subacute 
pulmonary tuberculosis, or in progressive cases with complications, 
such as those suffering from diabetes, tuberculosis of the kidneys, etc., 
in addition to the active pulmonary lesion, it is often advisable to 
console the unfortunate and doomed patient if he likes it, by telling him 
that the prognosis is excellent. 


1 Practitioner, 1913, 90, 38. 
2 Handbuch der Therapie, 1910, 3, 205. 


RELATION OF PHYSICIAN TO PATIENT 679 


Economic and Social Conditions.—In outlining the treatment to be 
pursued, the social and economic condition of the patient are always 
to be borne in mind. I/¢ 2s not advisable to tell a patient of limited 
means that a certain private sanatorium, or a climatic resort in a distant 
part of the country, 1s good for him. He is likely to brood over the 
fact that owing to his poverty he is lost, when in fact he could get 
along very well at home or in the neighborhood of his city. Well- 
to-do patients may be sent out of town with only suspicious symptoms 
and signs of the disease on the principle of some physicians to treat all 
“suspects” as tuberculous until proved to be free of the disease. The 
rest during the vacation does them good; in fact, they usually need 
it. But patients with limited means should never be treated in 
this manner. In them only a positive diagnosis of tuberculosis should 
be the criterion for radical and costly treatment. 

Relation of Physician to Patient.—A great deal has been written 
about the relation of the physician and his tuberculous patient, and 
it has been repeatedly stated that the former must possess certain 
qualifications which, if taken seriously, would exclude 99 per cent of 
practitioners from the category of physicians competent to handle an 
ordinary case. According to one writer, the physician must possess 
no less than an extraordinarily strong personality, immense will-power 
to impress it on his patients, unusual teaching ability, fervent enthu- 
siasm and unremitting interest, etc., if he is to meet with success. 

Evidently these requirements are such as all ideal physicians should 
possess if they are to be fit for successful practice. The truth is that 
in most cases it is quite easy to gain the confidence and codperation 
of the patient, if this is at all obtainable. The main problem is to 
retain it for the long period of time it takes until the termination of 
the case. This is especially true of chronic phthisis which runs an 
undulating course with accidents (hemorrhages, fever, anorexia, etc.) 
which come and go unexpectedly, and are liable to shatter the most 
implicit confidence. This is one of the reasons why tuberculous 
patients, next to those suffering from venereal diseases, are the best 
prey for quacks and charlatans. 

My observations lead me to the conviction that the average tuber- 
culous patient can be easily managed and his confidence retained for 
an indefinite time when we appeal to his reason. It is a grave mistake 
of many superintendents of public sanatoriums who try to obtain the 
codperation of their patients by keeping them in constant fear of 
punishment—expulsion. As one patient told me, the superintendent 
inflicted severe punishment on patients for small infractions of the 
rules of the institution because for these dependent patients the only 
hope of recovery was the sanatorium. Such severity does not at all 
help along in gaining the confidence of patients. I know of public 
sanatoriums in which the patients are always coerced into obedience 
of the rules and to submitting to prescribed treatment, but they do 
not discharge the proper proportion of cured patients, and a very 


680 GENERAL MANAGEMENT OF THE CASE 


large number leave the institutions of their own volition before the 
physicians discharge them. 

To a certain extent the patient treated by his physician at home 
is more amenable to reason than those in public sanatoriums. ‘The 
physician in private practice is in a position to individualize his cases 
and more easily persuade them that their only chances for recovery 
lie in their implicit obedience to orders. When the patient is told 
the reason why we want him to rest the greater part of the day for 
weeks or months; why we want him to eat certain kinds and quanti- 
ties of food; why we want him to submit to the operation for artificial 
pneumothorax, etc., he is more likely to submit than when we threaten 
him. All this can be done with alleged ignorant patients, who usually 
have more common sense than they are credited with, as well as with 
the intelligent and cultured. In fact, the former are, as a rule, more 
tractable than the latter. We must always remember that these 
patients make great sacrifices for months, and need consolation and 
encouragement which only the reasonable physician is able to bestow. 

Personal Hygiene.—The first instructions given to the patient are 
as regards his personal hygiene. This can best be done only after 
careful inquiry into his daily habits which, as a rule, are found not 
to have been exemplary; otherwise he would not have been likely 
to develop phthisis. To be successful, it is necessary to enter into 
the smallest details of every-day life, and most patients appreciate 
it greatly. 

Treating patients in cities, after deciding against a sanatorium, it 
is of immense importance to ascertain their home surroundings. A 
call should be made at the house of the patient to see whether it is 
fit for a tuberculous individual, and especial attention should be paid 
to the location of the sleeping room, its size, windows, exposure, etc. 
In case these are not found satisfactory, moving should be urged, 
preferably to the outskirts of the city or a suburb. Details are given 
in Chapter XX XVII. 

In our attempts at adapting the patient’s mode of life to the thera- 
peutic indications, we meet with great obstacles when trying to impress 
him with the urgency of cessation of work, physical and mental, and 
it is particularly difficult to persuade patients with mild lesions show- 
ing few constitutional symptoms. They are convinced that work 
does them no harm. The poor point to the necessity for providing 
for themselves and those dependent on them, while the well-to-do 
are apt to be even more intractable in this regard. They must not 
neglect their business, they must finish some task they have under- 
taken, they are deeply absorbed in some studies; they must continue 
at college until graduation, etc. But the careful physician is not 
moved by these pleas and points out to the patient that just because 
he is in such good physical condition the prognosis is so good. But 
should he continue working physically or mentally, the disease will 
surely make inroads on his vitality and the chances of ultimate and 


PERSONAL HYGIENE 681 


complete recovery will vanish. Whether he leaves the city or not, 
the patient may be induced to take a complete vacation with all the 
separation from the activities of life a vacation entails, but without 
any of its pleasures. The details about rest and exercise are given in 
i hapter XXXVI. 

Baths.—The mortal fear for “colds” entertained by many is accent- 
uated as soon as the diagnosis of tuberculosis is made and one of the 
first results is that the patient ceases to bathe. In many advanced 
cases, or even In incipients who suffer from profuse nightsweats, large 
patches of pityriasis versicolor are to be seen on the skin of the neck 
and trunk. When told that bathing will remove it, women are easily 
induced to take frequent baths. But all are to be instructed that 
bathing improves the circulation, activates the skin, and invigorates 
the individual. It must be insisted upon that the patient “bathes 
frequently and follows it up by vigorous rubbing of the skin with a 
rough towel. 

The question of cold baths in tuberculosis has been very much 
debated. In some institutions, cold baths and frictions are the chief 
elements of the cure. They are urged for the purpose of hardening 
the body against colds. But many are not fit for the purpose of 
hardening; they do not react properly and, instead of feeling refreshed 
and invigorated after a cold bath, their extremities are livid, benumbed, 
chilled, and they feel altogether miserable. These patients, indepen- 
dent of their physical condition, are better off when taking only warm 
baths, twice or thrice weekly, followed by frictions. The statements 
of some that every tuberculous patient can be subjected to a process 
of hardening, if methodically applied, does not hold, as is evident 
from the fact that it is not pursued systematically in most sanatoriums. 
Bed-ridden patients may be sponged with tepid, or even cold, water 
during febrile attacks with great benefit. Patients who have been in 
the habit of taking cold baths, douches, or sponging, every morning 
should continue to do so during their illness, but those w ho do not 
bear these procedures well should only bathe in warm water, as was 
just stated. 

Robust patients may also be allowed swimming within reasonable 
limits; bathing outdoors, especially sea bathing, is good for quiescent 
eases. Turkish and Russian baths are decidedly har mful in active 
cases. 

Clothing.—The tuberculous patient should be sensibly clothed, the 
aim being to keep him warm during the cold winter, but not over- 
heated. The fear for “colds” is responsible for the excessive under- 
wear which we often find on patients, and, coupled with the several 
vests, sweaters, coats and overcoats, they are often fairly borne down 
by the weight of their clothing. The well-known red flannel pad, “the 
chest protector,” has not as yet been abandoned after all the medical 
agitation against it; we often see patients wear them, and every drug 
store sells them. Not only do the poor and ostensibly ignorant classes 


682 GENERAL MANAGEMENT OF THE CASE 


make use of them but we meet them among so-called educated patients. 
They become habituated to this excessive covering of the chest, and 
perspire freely. When they attempt to remove it they are easily 
chilled, which is responsible for many of the catarrhal complications 
which occur during the course of the disease. 

In the beginning of the treatment, the patient is to be discouraged 
from such practices. He is to be told with due emphasis that woolen 
underwear, of thickness consistent with the season of the year and other 
meteorological conditions, is all that is necessary. A woolen garment 
has a capacity for absorbing considerable moisture without feeling 
wet, while cotton soon becomes saturated with moisture. If evapora- 
tion takes place suddenly, the body is chilled. Some patients are 
unduly irritated by wool next to the skin, but by constant wear they 
overcome this difficulty. Of course, it is important that the underwear 
worn during the day should not be worn during the night. 

All sudden changes in temperature within and out of the house are 
to be met by changing the overgarments. During the winter a fur 
coat is good, and can be purchased for about the same price as a good 
overcoat. Those taking outdoor treatment on a reclining chair need 
extra wraps during the winter. Carrington! gives a complete descrip- 
tion of the various appliances which may be used for the purpose. 

Women are less easily managed in regard to clothing than men. 
The low cut around the neck and chest is very harmful to tuberculous 
women, and they are to be induced to forego some of the fashions in 
vogue. But what is of most importance is the corset which many 
refuse to part with, claiming that it is not at all the figure they care 
for, but that they have been habituated to stays and feel uncomfortable 
without them. But when explained in detail the way a corset, even of 
those called “hygienic,” interferes with the respiratory movements 
of the thorax, most women submit to the argument. 

Smoking.—The problem whether a patient who has been found 
tuberculous should give up smoking has troubled many physicians 
in sanatoriums. Some have been inclined to prohibit it indiscrimi- 
nately and failed, as a rule. One who has been habituated for long 
years to smoking cannot easily give it up, and when he does he is 
often so nervous and miserable that it has an immense influence on 
his general well-being and the course of the disease. The fact is that 
smoking has no deleterious influence on the tuberculous process in the 
lungs, and there is no reason for imposing an additional hardship on 
the patient. Of course, chewing tobacco should be prohibited. 

The assumption that smoking predisposes to tuberculosis and 
aggravates the pulmonary condition if indulged in by tuberculous 
individuals, has been shown to be incorrect. Gerald B. Webb,’ in a 
statistical investigation, found that of a comparatively large number 
of soldiers in the United States Army, the proportion discharged from 


1 Journal of Outdoor Life, 1912, 9, 262. 
2 Am. Rev. Tubere., 1918, 2, 25. 


PERSONAL HYGIENE 683 


active service because of active pulmonary tuberculosis was no higher 
among those who smoked than among those who did not. His con- 
clusion that inhalation of the smoke of cigars or cigarettes does 
not predispose the lungs to tuberculous disease confirms this fact 
which has been long ago observed by clinicians. Webb, however, 
found that but few non-smokers have rhonchi, or sibilant rales, while 
the majority of smokers do present these signs of bronchial irritation. 
But as has been pointed out by Krause! in this connection, inflamma- 
tory processes have not been found to be predisposing factors for 
bacterial infection; they may rather be considered factors in the 
resistance against infection. William S$. Duboff? found that tobacco 
does not predispose to laryngeal tuberculosis, and that throat com- 
plications are no more frequent in tobacco users than in those who 
use no tobacco. Laryngitis, of specific character or not, appears to 
be equally as common among women as among men in the course of 
pulmonary tuberculosis, showing that tobacco is not an important 
factor. 

When there are laryngeal complications smoking is apt to cause 
irritation and cough. However, I am inclined to follow Fetterolf’s* 
suggestion: The patient, if he craves for his cigar, cigarette, or pipe, 
is thus instructed: ‘The smoke is not to be blown through the nose 
or inhaled; that if a cigar or cigarette is used it shall be smoked in a 
holder at least four inches long, and, finally, that the smoking be 
done in the open air. The main evils, barring excess, are dry heat 
and dust which are drawn into the pharynx and larynx. ‘This is of 
greater significance the shorter the smoked article grows, and if the 
cigar or cigarette is used in a holder and only the first half is smoked, 
this evil is largely done away with.” It is Fetterolf’s belief that with 
such precautions as just mentioned and with the smoking done in the 
open air, no harm will result. A non-smoking patient in a close room 
with others smoking is at a greater disadvantage than one who is 
smoking in the fresh air. 

Occupation.—A great deal has been said of occupations fit for tuber- 
culous patients. The problem is not one which concerns those with 
active disease, but the convalescents, as well as those who have recov- 
ered. A patient during the active course of phthisis in any stage 
should have no occupation at all. He cannot work, he must not attend 
to any vocation which requires physical or mental exertion. Mistakes 
are often made in permitting patients in the incipient stages to wind 
up their business, to finish a course in a school, ete. This is a point 
which will be discussed later on while speaking on rest and exercise 
and cannot be emphasized too strongly. 

It is very difficult to advise patients who have recovered from phthisis 
as to their future activities in the affairs of life. With the rich and 
prosperous the matter is very simple: They may be allowed to return 


1 Am. Rev. Tuberc., 1918, 2, 99. 2 Dldso 2; ale 
3 Hare’s Modern Treatment, 2, 405. 


684 GENERAL MANAGEMENT OF THE CASE 


to their vocations provided they know how to take care of themselves. 
Under supervision, and with careful observation of the ordinary rules 
of healthy life, they very often avoid relapses. The same is true of 
professional people who can resume their life work, perhaps at a slower 
pace. But with those who have been artisans, manual laborers, ete., 
especially in “precarious occupations,” the matter is different. It is, 
indeed, easy to advise one to change his vocation, as is done in sana- 
toriums when patients are discharged, but whether the patient is more 
harmed by working at his trade and earning for his support, than by 
starvation because of lack of funds to buy food, pay for his lodging, 
etc., is hard to decide. 

Moreover, a change of occupation is not feasible in the vast majority 
of cases, especially with skilled artisans. They cannot easily accept 
iow wages when at their own trade the pay is much higher, and the 
hours shine ter. It is also a fact, only rarely considered by medical 
men, that the artisan has usually adapted his organism to his peculiar 
occupation; in fact, there is a process of selection going on, certain 
persons are attracted to certain trades at which they succeed. ‘They 
must return to these occupations after recovering from the disease, 
if they are at all to be able to support themselves. And they do, in 
fact, in spite of our protestations. 

But we must try to keep convalescing tuberculous patients from 
hard muscular exertion, if relapses are to be avoided. They are to 
be under medical supervision for several months after beginning to 
work, and if they show any signs of damage to their constitution, 
especially fever, dyspnea, tachycardia, etc., they must stop before 
it is too late. Nor should a cured patient be allowed to work at any 
dusty trade, such as pottery and earthenware manufacture, cutlery 
and file making, certain departments of glass making, copper, iron, 
lead and steel manufacture, stone cutting, textile trades, fur- or cigar- 
making, iron-grinding, etc. We have seen the effects of organic, 
mineral, and metallic dust in the direction of engendering a soil suscep- 
tible to phthisis. When we bear in mind that a patient with cured 
tuberculosis almost always harbors virulent tubercle bacilli in the cica- 
trized area of the lung, we can easily understand that irritating dust 
may at any time flare up a dormant lesion into renewed activity or 
cause metastasis. 

Tt is always to be remembered that farming is not the only outdoor work, 
nor is it the best. Farm laborers usually work very hard for long hours, 
small pay, and with food that does not satisfy the majority of city 
dwellers. In addition, as has been pointed out by Vogeler,! the lack 
of amusement during the hours of recreation and the enervating heat 
during the summer are serious drawbacks. Of course, it is different 
when the patient can raise funds to buy or lease a farm for himself. 

There are in cities many more or less remunerative occupations 


1 Trans. Nat. Assn. Study and Prev. Tuberc., 1912, 8, 113. 


PERSONAL HYGIENE 685 


which are suitable for this class of cases, as conductors, motormen, 
ticket agents, attendants at ferries, watchmen, solicitors, ete. My 
observations lead me to the conviction that workers at the garment 
industries, excepting at fur, may safely return to their occupations, 
provided they find employment in light and well-ventilated workshops. 
The same is true of the building industry, provided the exposure to 
the vicissitudes of the weather is not excessive nor the hours too 
long; and of clerks, salespersons, ete. Indeed, I have been struck 
with the fact that when a patient who recovered from phthisis 1s unable 
to pursue the vocation for which he has been trained for many years, he 
will not do well, even if he remains idle indefinitely. 

In advising tuberculous convalescents about occupations, the fact 
must not be lost sight of that we know very little about the subject. 
We have shown that only certain kinds of dust predispose to phthisis, 
while others, on the contrary, apparently confer more or less immunity 
against the disease. Among the latter may be mentioned coal dust, 
lime dust, ete. (see p. 132). The same is true about the problem of 
indoor as compared with outdoor occupations. When we find that 
hotel servants have a very high mortality from tuberculosis, it does 
not necessarily mean that it is because of their indoor work. On the 
one hand the work, not involving strong muscular exertion, attracts 
weaklings, and then also they are liable to drink excessively. Street 
sweepers are apparently spared by tuberculosis to some extent, but 
their outdoor occupation also involves the inhalation of dust exces- 
sively. I have seen very few tuberculous patients among the workers 
in the underground subway of New York City despite the fact that they 
are employed in an indoor occupation par eacellence. The same has 
been noted in London. Cobbett! mentions that the old underground 
railway in London, before it was electrified, was considered as a par- 
ticularly favorable place for consumptives. The stations of Portland 
Road and Gower Street, which were entirely below the surface of the 
ground, and which were formerly notorious for their mephitic vapors, 
were regarded as the best for tuberculous patients, and the authorities 
transferred to these stations any of their workers who showed signs 
of incipient tuberculosis. The problem of “indoor,” as compared 
with “outdoor” occupations is thus seen not to be as simple as some 
believe it is as regards tuberculosis. 

In judging a patient with a view of selecting an occupation for him, 
we may be guided by the condition of his temperature, pulse, respira- 
tion, and general constitution, but the extent of the lesion is a hazard- 
ous criterion. All who have had experience agree with H. M. King 
that “it frequently happens that a satisfactory condition of health 
as determined by restoration of working efficiency maintained for many 
years is not incompatible with physical signs which of themselves 
would indicate active disease.” I have seen many cases in which the 


! Causes of Tuberculosis, London, 1917, p. 98, 


686 GENERAL MANAGEMENT OF THE CASE 


reverse was true, the patient showed no signs of active disease in the 
lung, yet as soon as he began to work he broke down with fever, rapid 
pulse, dyspnea, etc. These patients cannot work at all. Then there 
are others who will work for several months and, owing to an evanes- 
cent, acute, or subacute exacerbation, are laid up for several days or 
weeks. With these it is very difficult to judge the ability to work. 
All tuberculous patients, even after completely recovering from the 
disease, find it difficult to compete with healthy persons, but the 
class just mentioned is more apt to lose in the struggle for existence. 
They must find for themselves employment of a nature which makes 
them independent of strict regularity. 

On the whole, i appears that cured patients do best when returning 
to their old vocations for which they have been trained, and at which they 
can earn the most with the least possible effort. It may be said that, 
with some striking exceptions, uf a patient rs not able to pursue his former 
line of work he is altogether disabled. 


CHAPTER AX XVI. 
THE REST CURE. 


Principles of the Rest Cure.— Nature makes a strong effort at repair- 
ing the affected lung in tuberculosis, but we only rarely appreciate the 
method it pursues while doing it. Examining the chest of a tuber- 
culous patient, we find on inspection that there is a strong tendency to 
putting the affected area of the lung at rest. As already has been 
shown, during the early stage the muscles overlying the pulmonary 
lesion are almost invariably rigidly and spasmodically contracted. 
This contraction has been ascribed by Rubel! to the physiological 
coordination of the respiratory. center. It inhibits or prevents the 
motion of the underlying diseased lung to a certain extent. Later, 
pleural adhesions are formed which impede the respiratory movements 
of the lung to a yet greater extent, as is seen in the lagging of the 
affected side of the chest, offering favorable conditions for cicatriza- 
tion. ‘This immobilization of the affected part of the lung also slows 
the circulation of blood and lymph in that area, retains the bacteria 
and their toxic products, thus lessening toxemia and preventing 
metastatic auto-infection of unaffected parts of the lung. Rubel has 
shown experimentally that functional rest greatly contributes toward 
a cure of tuberculous lesions in the lung. He immobilized one lung 
in rabbits and then infected them by the intravenous way. In the 
relatively immobilized lung the lesion was found to be of the chronic 
and favorable variety, while in the freely movable lung it was acute 
and progressive. 

Surgeons have utilized physiological and functional rest in the 
treatment of tuberculosis of bones and joints. The modern treatment 
of Pott’s disease, and tuberculosis of joints in general, consists mainly 
in affording rest to the affected parts. The splint has done better 
than the knife in these forms of tuberculosis. Formerly physicians 
aimed at procuring rest in tuberculous diseases of the thoracic viscera 
by the application of strips of adhesive plaster, thus immobilizing the 
thorax; and at present the induction of an artificial pneumothorax 
puts the affected lung at complete functional rest. “In breathing, a 
normal person ‘opens and shuts’ the lungs nearly 30,000 times a day,” 
says Webb. “By rest we aim to make the breathing as shallow as 
possible, imitating almost that of hibernating.”’ 

In febrile cases rest has a rationale which is clear to everyone who 
gives some thought to the subject. Fever is an indication of activity 


1 Ztschr. f, Tuberk., 1908, 10, 193, 319; Roussky Vratch, 1907, 6, 648, 721, 750, 896. 


688 THE REST CURE 


of the tuberculous process and results from absorption of toxins and 
decayed lung tissue. By keeping the patient at rest we reduce the 
frequency and depth of respiration, and thus less of the toxins are 
washed into the blood stream and the fever declines. Fever also means 
increased metabolism and we must not further increase it by exercise. 
With the reduction in the fever there is an amelioration in the cough, 
and an improvement in the appetite, resulting in better nutrition of the 
patient. 

Rest and Exercise in Phthisis.—In former days the treatment of 
tuberculosis consisted mainly in removing the patient to some country 
place, or better yet, to an institution, and urging him to exercise in the 
open air. Thus, the main principles of the treatment in Brehmer’s 
sanatorium were outdoor exercise for long hours, daily walking, driving, 
horseback riding, mountain climbing and respiratory exercises. The 
same methods were followed in institutional and home treatment 
by many physicians until about thirty years ago. 

The development of sanatoriums in which careful observations have 
been made on the effects of these exercises on tuberculous patients 
has resulted in swinging the pendulum, and rest has come to the fore- 
ground as the most important factor in combating the disease, so that 
at present vigorous protests are heard from many sides that the indo- 
lent life led by sanatorium patients is often more harmful, for various 
reasons, than the exercises which were formerly in vogue. Indeed, 
Paterson reports just as many cures at Frimley, where the patients 
do graduated work, as in sanatoriums in which they are kept at perfect 
rest for long months, or even years. Moreover, a curious phenomenon 
is to be observed in most sanatoriums: The physicians, nurses, etc., 
are mostly recruited from the ranks of the tuberculous. They all work, 
more or less. Yet, on the whole, they are doing better than the 
patients who take the rigid rest cure. Of course, they are a select 
group, with chronic lesions. But patients with such lesions and 
activity are often kept at the rest cure for exceedingly long periods of 
time. 

The contradictory evidence in favor of rest or work is obviously 
due to the fact that neither rest nor exercise is a panacea which will 
help in every case, but that each has its indications and contraindica- 
tions. When patients presenting symptoms of active and progressive 
phthisis—fever, anorexia, emaciation, etc.—are urged to work or 
exercise, considerable harm is often done, and a favorable case may 
thus be converted into one which is decidedly hopeless. In the later 
stages of the disease, when the lesion has localized itself and the patient 
has no fever, eats well and feels strong enough to do some work, perfect 
rést nay-be-distinetly harmful, as will be pointed out later on. Rest 
and exercise have their indications and contraindications. 

Indications for Rest.—Nature puts most patients who suffer from 
active and acute forms of the disease at rest. They are weak, anemic, 
emaciated, and the exhausting cough, the dyspnea, and the phenom- 


REST AND EXERCISE IN PHTHISIS 689 


ena of toxemia in general, preclude any kind of exercise. But in the 
chronic cases, or even in some of the subacute cases, the patient may 
not realize his plight and continue working at his occupation until 
he breaks down, when it is too late to recoup the lost flesh and forces. 
Rest, properly applied, in this class of cases may prove life saving. 

It is clear that all active cases with fever, tachycardia, anorexia, emacia- 
tion, weakness, etc., are to be kept strictly at rest until most of these symp- 
toms have disappeared. It must be stated at the outset that the extent 
of the lesion is no reliable criterion as to the indications for rest and 
exercise. A patient in the incipient stage, with a limited and circum- 
scribed lesion at one apex, and suffering fr om fever, dyspnea, anorexia, 
etc., is often more harmed by work or exercises than one in the 
advanced. stages, with extensive involv ement of both lungs, but with 
normal pulse and temperature. 

With but few exceptions, the rate of the pulse is as good an index 
of the fitness of the patient to work as there is. So long as it is 90 or 
over per minute, or it is accelerated to that rate by mild exercises, the 
prognosis is not good, unless the patient is kept at perfect rest. In 
tuberculosis we often meet with unstable tachycardia; the pulse runs 
up to 120, or more, per minute at the least exertion or excitement. 
Such patients are to be kept in bed, or on the reclining chair, until we 
find that mild exercise, like walking slowly on level ground for a half 
or one mile, does not unduly accelerate the pulse. Some of these cases 
with tachycardia are afebrile, the temperature is in fact very often 
below normal, and exercise may not affect it, but the pulse is accel- 
erated on the least exertion. 

Dyspnea, when present, 18 another sign that the patient must be kept 
at rest. We must be guarded and not wait for subjective dyspnea, 
because many tuberculous patients have adapted themselves so well 
to their difficulties in breathing that they are not much disturbed 
by it, and when seen to breathe very superficially and rapidly, even 
more than thirty times per minute, they may inform us that they 
suffer no inconvenience in this respect. It is objective dyspnea which 
should guide us in our estimation of the effects of rest or exercise in 
tuberculous patients. Likewise, acrocyanosis is not to be taken as a 
sole criterion. Many tuberculous patients with healed lesions remain 
with bluish finger nails due to vasomotor disturbances. In some of 
these patients the circulation, while below par, is fair enough for 
ordinary activities. 

Fever has been considered an indication for rest by most writers 
on the subject; in fact, the problems of exercise and rest have usually 
been solved by the thermometer./ In cases of tuberculosis in which 
the temperature reaches 100° F. the patient is put to bed, and kept 
there until it descends to normal. In acute cases, with continuous 
fever, or during acute exacerbations in chronic cases, or when some 
complication ensues, such as pleurisy, or any non-tuberculous infection, 
complete rest is enjoined until the fever abates. In far-advanced cases 

44 


690 THE REST CURE 


with hectic fever, reaching a high degree in the afternoon or evening 
and dropping to normal, or even below, in the early morning hours! 
the patient is to be kept in bed at absolute rest. There are, however, 
cases of tuberculosis with fever which do not require strict rest. They 
are discussed in detail elsewhere, while speaking of the treatment of 
fever. It may be stated here that the body of many tuberculous 
patients adapts itself to the temperature, and moderate rises may not 
at all disturb them. In fact many of this class of patients do better 
work when the temperature is one or one-and-a-half degrees F. above 
normal. 

Technic.—The rest cure, when indicated, is to be carried out 
methodically. In acute progressive cases it means complete rest in 
bed until the temperature declines to below 100° F. Some patients 
revolt, saying that they feel strong enough to walk around for several 
hours of the day, that they are lonesome and would surely improve 
if they were permitted to assume the erect position for some time. 
But they are to be told that fever cannot be cured outside of the bed, 
and as Poujade said: “Undoubtedly prolonged rest in bed weakens 
a patient, but 1t weakens less than fever, which kills.”’ 

In the home of the patient it is advisable, when feasible, to have 
two beds, in one of which he sleeps during the night, and in the other 
he spends the day. Considering that the: patient may have to remain 
in bed for weeks or months, the enforced solitude is hard on him, 
and the change of the bed has some salutary effect. Moreover, these 
patients are apt to sleep during the day and suffer from insomnia during 
the night. One of the reasons for sleeping during the day is the 
extreme to which the rest cure is often carried. The patient is pro- 
hibited from reading, or accepting visitors. There is no reason for 
these prohibitions in those with mild fever, especially in tuberculosis 
which does not strike the patient down to the same extent as fevers 
due to other causes. By changing the room and bed they often be- 
come habituated to sleep in one bed, and remain awake during the 
day in the other. One room and bed may also be aired while the 
other is used. 

In the morning, when the patient wakes, he is to be given a sponge 
bath—one with alcohol is invigorating—and dressed, the lower half 
of the window opened and the bed placed in such a position that he 
can look out on the living world. If he feels cold, a hot-water bag 
should be placed at his feet. Great care must be taken to prevent bed- 
sores In prolonged and advanced cases. 

When the temperature descends below 100° F.; in prolonged cases 
when it reaches this degree only at a certain time in the afternoon, 
but is near normal during the rest of the day, the patient may be 
kept at rest on a reclining chair during the greater part of the day, 
preferably outdoors, and reading and ila games may be allowed; 
only during the hours when the rise in temperature is expected is he 
to be made to go to bed. When we find that this does not increase 


af 


REST AND EXERCISE IN PHTHISIS 691 


the fever, he may be permitted mild exercises, such as short walks, 
and the effects should be watched. We are often surprised to find 
that the fever disappears altogether with mild exercises. I have 
observed this to be the case when walking promotes expectoration. 

This rest in bed is at times very difficult to carry out. The poor are 
often working for weeks while the temperature is high—I have seen 
them wor king with fever of 103° F., and even higher. When beyond 
control in this regard, the patient is to be sent to an institution, or 
to one of the day and night camps. I have seen excellent results in 
such cases after the patient has been at one of these institutions 
for afew months. Not only has the fever disappeared, but the patient 
was educated to appreciate the dangers of exercises during the febrile 
stage. But the well-to-do are not better in this respect. Very often 
we find them walking around, and even dissipating, in spite of the 
fact that their temperature is above 102° F. Indeed, they are often 
less amenable to reason in this respect than the poor. They are to be 
impressed that all business and pleasures are to be given up when the 
temperature is high. 

Contraindications.—It was one of the great mistakes of many sana- 
toriums to urge all patients to keep at perfect rest and abstain from 
work or exercises, irrespective of the form of the disease and the 
constitutional symptoms. The result was that they turned out lazy 
people—hypochondriacs—who feared work, and who at the least 
fatigue considered themselves harmed by it after they had been cured. 
In most sanatoriums of today strong efforts are being made to avoid 
such mistakes. 

As was already stated, the extent of the lesion is not always an 
index as to the indication for rest. There are many patients with 
extensive lesions in the lung, in fact with large excavations, who are 
well able to make themselves useful along certain lines. Inked, _ there 
are cases In which prolonged rest is distinctly harmful. The nervous 
system may be functionally damaged beyond repair, the desire for 
activity may be stifled, and the resistance of the body in general may 
be lowered. H_has-alse-been-strggested-byPaterson-andimanthet 
prolonged. rest depriv es the patient of certain reactions which bodily 
activity calls forth in the pulmonary lesions, and w hich are of great use 
in combating the deleterious effects of the disease. 

In some sanatoriums where the rest cure has been carried to excess 
we often meet with patients who, after remaining in bed or on the 
reclining chair for several months, become mentally tired and listless; 
they lack interest in current affairs; other become hypochondriacs, 
consulting the thermometer several times a day and are alarmed at 
each finding above or below normal. ‘They often lose all hope of ever 
getting cured and this despondency contributes greatly to the unfavor- 
able course of the disease. Having met many patients with the 
“thermometer habit,” I have often regretted the invention of this 
instrument of precision. 





692 THE REST CURE 


The graduates of sanatoriums in which the rest cure is carried to 
excess are apt to be lazy for the rest of their lives. Some of them, 
discharged from one institution, immediately seek admission to another. 
As Herman M. Biggs says, “A sick workman is converted into a 
healthy loafer.” They fear muscular exercise of any kind and imagine 
that the least work aggravates their condition. In the State and 
municipal institutions in this country we find many with a record 
of having been in several sanatoriums. In fact, prolonged rest di: - 
ables any human being, because the joints become stiff and any 
attempt to walk produces muscular weakness, pains and aches in 
the limbs. In some, the long rest favors the deposition of fat, which 
is very encouraging, but when carried to excess, which is not a very 
rare phenomenon among the tuberculous, it may disable the patient 
as much as active phthisis. These patients must have’ exercises to 
reduce the fat. This is mainly seen in patients in whom the disease 
may or may nor be active, but at any rate is not progressive; the lesion 
has become quiescent, completely surrounded by connective tissue. 
Rest may only produce obesity of various degrees, but does not assist 
in the healing of the disease focus in the lung. It is in these cases 


that graduated work or any exercise will do more than rest, and ae 4 


VicLeanis-nphorism; “Tf the phthisical patient would live, he must 


work for it,” is Sonnemied 

Exercise.— When the temperature and pulse become normal and 
remain so for several days, walking exercises are to be commenced, 
with a view of preventing the deleterious effects of idleness, as well 
as provoking mild reacti hich are, in most 
‘ases, of immense benefit. At first the patient is allowed to walk a 
mile on level ground and the effects on the temperature and pulse are 
watched. It may be done during the morning hours, when the tem- 
perature is normal, while in the afternoon, when there is some fever, 
the patient is ordered to rest on a reclining chair, or even in bed. But 
in those in whom the afternoon temperature is mild, below 99° F., 
even this precaution need not be taken, provided the pulse is below 
85 per minute. 

The following schedule for walking exercises, modified after that 
given by E. Hyslop Thomson,! may guide the patient who takes his 
own temperature: 





99.0; short walk. 
99.5; rest outdoors or short walk around house. 
100.0 or higher; remain in bed. 


Morning temperature 


| 98.5 or lower; long or medium walk. 
at 7 A.M. | 


99.5; short walk. 
100.0 or higher; rest in bed or reclining chair. 


99.0 or lower; medium or short walk. 
Temperature at noon 


Evening temperature f{ 99.5; only short walk on the following day. 
at 7 P.M. | 100.0 and above; complete rest during following day. 


' Consumption in General Practice, London, 1912, p. 223. 





GRADUATED LABOR 693 


Hill climbing, or walking long distances, up to fifteen miles a day in 
afebrile cases without tachycardia may be permitted. The author has 
thus tested patients as to their ability to work, and was surprised to 
find often that they were rather invigorated by the exercise and they 
were then allowed to work for their support. Our patients are told 
to come to the office on foot, walking a mile or two, and if when they 
arrive the pulse and temperature are found normal, they are told to 
walk a longer distance the next day, etc. When this test shows that 
no harm is done by the exercises the patients are allowed to work, 
first under supervision, and later completely discharged with instruc- 
tions as to the signs of danger. 

Graduated Labor.—Practitioners among people in large cities are 
often impressed with the capacity for work of many consumptives 
amid unfavorable surroundings for years without visible harm. Among 
these cases there are many who are evidently active but not progres- 
sive: some are entirely quiescent. We must repeat that the extent 
of the lesion is less of an index as to the capacity for work than its 
activity as revealed by the constitutional symptoms, such as fever, 
tachycardia, dyspnea, etc. Paterson’ developed his system of gradu- 
ated labor after observing such cases in England. “It occurred to 
me,” he says, “that if some consumptive persons under adverse cir- 
cumstances and without any medical guidance could act thus without 
apparent injury, they ought, under ideal conditions and with the work 
carefully graduated in accordance with their physical state, to be able 
to undertake useful labor. On this assumption manual work should 
be of great advantage to patients undergoing treatment in a sanatorium, 
as at first it would do much to meet the objection that members 
of the working classes are liable to have their energy sapped, and 
to acquire lazy habits by such treatment; second, it would make them 
more resistant to the disease by improving their physical condition; 
and third, it would enable them by its effects upon their muscles to 
return to their work immediately after their discharge.” 

With a view to developing the muscles of the upper limbs, which 
are supposed to have more direct influence on the expansion of the 
lungs, Paterson? is not satisfied with walking alone. When a patient 
is found to be able to walk two miles a day without aggravating his 
condition, he is given a basket in which to carry mould for spreading 
on lawns, ete. No case of hemoptysis or of pyrexia occurred among 
these patients. When they have been on this grade with nothing 
but beneficial results for from three weeks to a month, they are 
given boys’ spades with which to dig for five minutes, followed by an 
interval of five minutes for a rest. After a few weeks, several of the 
patients on this work, who were doing well, were allowed to work as 
hard as possible with their small spades without any intervals of rest. 
As they had all improved on this labor, larger shovels were obtained, 


1 Sixth Intern. Cong. Tuberc., 1908, 1, 886. 
2 Thid,, 901. 


694 THE REST CURE 


and it was found that these patients were able to use them without 
the occurrence of hemoptysis or of a rise in temperature. About this 
time many of the patients were feeling so well that it became neces- 
sary to restrain them from doing too much. 

Paterson worked out a schedule for graded work which brought 
excellent results. It was noted that many patients on their arrival 
are somewhat remarkable for a somewhat sullen and apathetic attitude, 
but as soon as their physical condition undergoes amelioration, all 
traces of gloom and depression leave them and they become lively, 
cheerful individuals. In many cases in which the improvement was 
not prompt, the effect of harder work was tried and often a progressive 
improvement was noted at once. Paterson found that the danger 
signals are: a temperature of 99° F. or higher in men and 99.6° F. in 
women, loss of appetite and slight headache. As soon as these appear 
the patient is to be put to bed until the temperature goes down to 
normal. In my experience, a rapid pulse is of even more importance 
as an indication that exercises are deleterious. 

Inman, working with Wright’s method of ascertaining the opsonic 
index in patients under this graded work system of Paterson, found 
that it was at some part of the day well above normal and he explains 
it as due to the stimulus supplied by the work, inducing artificial 
auto-inoculation; that the organism responds by the production of 
immune bodies. In fact, whenever excessive auto-inoculation takes 
place harm is done. This, he points out, must be readily recognized 
clinically if harm is to be avoided. “A patient doing well on the 
grade of work prescribed for him and with no abnormality of tem- 
perature suddenly complains of feeling tired, of loss of appetite and 
of headache; and the temperature chart registers an elevation to 
99° or 100° F. These are precisely the symptoms which are found 
during the negative phase after excessive dose of bacterial vaccine.” 

Paterson is guided in his conduct of a case by the thermometer, 
and whenever the temperature registers 99° and over in men and 99.6° 
in women (by mouth), the patient is kept strictly in bed. When 
work has been assigned, the temperature is watched, and so long as 
it is not increased by the exertion, the work is increased in duration 
and intensity. Even afebrile patients who are of poor general condi- 
tion are not allowed to work, but kept at perfect rest, excepting that 
they are allowed to walk to and from the dining hall for their meals. 

It is thus evident that there is little new in this system of exercises 
and work. Physicians have always allowed their afebrile patients who 
are of good general condition and not easily fatigued to work and 
warned them to stop as soon as symptoms of toxemia, such as a tired 
feeling, weakness, debility, drowsiness, make their appearance. Intel- 
ligent patients have been given thermometers to guide them. 

Paterson’s method has, however, done a great deal for institutional 
patients by drawing attention to the importance of exercises and work 
in attempts at prevention of indolence which, in many cases, remains 


GRADUATED LABOR 695 


as a reminder of the disease and the institutional life to which they 
have been subjected. 

Outdoor Games.—Afebrile patients without tachycardia are to be 
encouraged to do some exercise in the open air, otherwise they are 
likely to brood over their troubles, and in some cases even harmed 
by obesity. Walking exercises alone are often insufficient to keep the 
average patient busy, and outdoor games are often good to help him 
pass his time pleasantly and to benefit the muscles, the appetite, and 
the metabolism. 

In advising a patient as to outdoor games we must always consider 
his life, habits, and customs before he took sick. Those who indulged 
in sports may be permitted to resume their favorite games, provided 
they do not raise the temperature, or produce breathlessness. This 
at once excludes certain games. “All violent sports should be 
avoided,” says Lawrason Brown. “Golf (without the full swing), 
croquet, fishing and hunting (not entailing too much exercise), gentle 
bicycle riding (on the level), rowing or paddling, skating (for those 
proficient), skiing, snow-shoeing, swimming (in great moderation), 
and horseback riding may be indulged in with moderation when the 
disease has been arrested.”’ 

It seems to me that of the outdoor games, golf is the best for patients 
who have just recovered from phthisis. Cricket, football, and athletic 
sports in general produce more or less dyspnea, while golf makes less 
violent demands on its votaries and is usually played in open, breezy 
places. However, those who perspire freely are at times greatly 
harmed by outdoor exercises. “Catching cold” is apt to reactivate 
quiescent lesions (see p. 125). Though in this bacteriological era 
many deny the etiological potentialities of colds and chills, experience 
has taught that they are factors for evil in many cases. 

Indoor Games.—The tuberculous patient is to be allowed some 
games for his amusement when he is kept indoors, excepting when 
the temperature is above LOO° F. and he is kept in bed during the 
whole day. I believe it is wrong to interfere with them when they 
play cards, checkers, and chess, as is often done in public sanatoriums, 
on the assumption that the excitement is liable to raise the temperature, 
provoke hemoptysis, etc. While it cannot be said that these games 
immunize patients against such accidents, I have never seen such 
results follow when they are allowed to have some amusement during 
the long, lonesome, days and weeks in the institution or at home in the 
sick room. 

Patients treated at home are not to be allowed to go to theaters, 
or other indoor and badly ventilated places of amusement so long as 
they have fever. 


GRAPE RIS Xe vee 
OPEN--AIR TREATMENT. 


Mosr writers state that Brehmer was the first to demonstrate, in 
1859 in his sanatorium, the great value of the open-air method of treat- 
ment of tuberculosis. But it is a fact that he had many precursors. 
In 1840 George Bodington, a country doctor in the village of Erding- 
ton, published an Essay on the Treatment and Cure of Pulmonary 
Tuberculosis, in which he vigorously protested against the close con- 
finement of consumptives for fear of the evil influences of cold, fresh 
air, “forcing them to breathe over and over again the same foul air 
contaminated with diseased effluvia of their own persons.” Arguing 
against the value of antimony, calomel, and bleeding, which were in 
vogue in those days, he urged the free administration of nutritious 
food and stimulants with plenty of exercise in pure and, if possible, 
dry, “frosty” air. In short, his great specific in phthisis was dry, 
cold air which, he said, had a most powerf] influence in “healing and 
closing of cavities and ulcers of the lungs.” 

Needless to say, he was severely handled by his contemporaries and 
so discouraged that he had to give up his method of treatment, con- 
verting his “sanatorium” into an insane asylum. Brehmer in Ger- 
many and Trudeau in the United States, later took up work along the 
lines of Bodington and met with no small amount of opposition and 
ridicule from the contemporary leaders of the profession and the laity. 

At present the gospel of fresh air needs no evangelists to bring it 
home to most sufferers from phthisis; it is the acknowledged corner- 
stone of phthisiotherapy. The only difference of opinion is where and 
how it can be applied most effectively. Some send their patients to 
certain regions where the climate is alleged to have a specific influence 
on the disease; others direct them to sanatortums where they may 
benefit by both the climatic advantages and certain therapeutic 
methods which are the hobby of the presiding genius. Many are con- 
vinced that similar advantages may be obtained at the home of the 
average patient. 

Where Open-air Treatment May be Obtained.— The open-air treat- 
ment consists in inducing the patient to live permanently in pure, 
fresh air, preferably outdoors or, when he must stay indoors, the air in 
the room is to be renewed constantly. There is no question but that 
this is best obtained in the country, or in a special institution. But 
most patients cannot afford to leave the city for an indefinite period, 
nor are there a sufficient number of institutions in any country to 


OPEN-AIR VS. CLIMATIC TREATMENT 697 


accommodate all active tuberculous patients with places for as long 
as the disease lasts. In fact, if all the patients were to decide that 
they want to submit to hospitalization for therapeutic or prophylactic 
purposes, it would be found that only a small fraction of the eligible 
could be accommodated. 

Says Edward Cummings:’ “Personally I.cannot see the need of 
banishing the tuberculous patient from his comfortable chamber to a 
shack in the back yard, or a woodshed, or a tent house in the dusty 
desert. One does not always have to go across the continent to get 
fresh air, not even out in the yard. . . . The ordinary bedroom 
for most persons is well enough.” My own observations in large 
modern cities like New York, Boston, Chicago, St. Louis, Philadelphia, 
London, Manchester, etc., have convinced me that results can be, 
and are, obtained which compare favorably with climatic and institu- 
tional treatment. Of course, in the congested districts and slums, 
the overcrowded tenements are even less suitable for consumptives 
than they are for human habitation in general. But there are dis- 
tricts in every city which can be utilized for the purpose of housing 
consumptives and the results attained will not be behind those attained 
after sending patients far away from their homes at great expense and 
often hardship. 

The suburbs around cities are suitable for families in which there 
are tuberculous members, and the expense involved in moving them to 
these parts is comparatively trifling; in fact, the rent is often lower, 
and they need not lose their jobs, or break up their business. The 
social and economic aspects of tuberculosis, which are but rarely con- 
sidered in this connection, assume a different aspect when the patient 
must not be sent far away from home, or from the place of employment 
of those he depends on. 

Open-air vs. Climatic Treatment.—These two methods must be 
kept distinctly apart. Experience has taught that there is no climate 
on the habitable globe in which consumption does not occur, or where 
a patient sick with the disease will surely recover, even when sent 
thither in the very incipient stage of the ailment. In the climatic 
resorts which have become popular—and it is a fact that the popular- 
ity of a region is by no means an index of its therapeutic efficacy—the 
patient must subject himself to a certain discipline, if he expects results. 
Irrational mode of life in the mountains or at the sea coast will aggra- 
vate the condition of a consumptive to the same extent as it will in the 
city. A healthful mode of life in any place will, and does, improve the 
condition of the average consumptive, no matter where he is. 

The treatment of tuberculosis in certain climatic regions, as we shall 
see later on, has its indications and contraindications, while home 
treatment has certain advantages in this regard. It can be applied 
successfully in the treatment of nearly all cases, in all forms of phthisis, 





1 Journal of Outdoor Life, 1912, 9, 257. 


698 OPEN-AIR TREATMENT 


and in all its stages; striking results are obtained in patients with 
limited means, as well as in those who are well-to-do; in febrile and 
afebrile cases; in hemorrhagic and cachectic cases; in those with or 
without gastric derangements. In short, in all cases of tuberculosis, 
in all its forms, in all stages of the disease, during any season of the 
year in almost any climate, except the arid. 

To be successful, it must be applied rigorously, methodically, and 
properly regulated by the physician. This is no more than institutional 
treatment depends on, excepting that the former is cheaper for the 
community which is charged with caring for its consumptives, and 
more attractive to many who have sufficient material means at their 
command. 

Dangers of Stagnant Air.—Our conception of the beneficial effects 
of indoor life has undergone radical changes during recent years. ‘The 
reasons why the stagnant air in a room occupied by human beings 
is harmful are not clear. Recent investigations by Leonard Hill, 
Haldane, Benedict, Fliigge, C.-E. A. Winslow, and others, have shown 
that it is not the excess of carbon dioxide, or the decrease in the pro- 
portion of oxygen which renders the stagnant air harmful. The 
most deteriorated air in a badly ventilated room never shows on 
analysis as much as 1 per cent of carbon dioxide, while in famous 
health resorts at high altitude there is a far greater deficiency of 
oxygen than can ever be found in the worst ventilated room. The 
specific organic poisons of human origin, the morbific anthropotoxins, 
of which some have spoken, have never been isolated. 

As Winslow! points out, recent studies indicate beyond any reason- 
able doubt that the more obvious effects experienced in a badly ventil- 
ated room are due to the heat and moisture produced by the bodies 
of the occupants, rather than to the carbon dioxide or other substances 
given off in the breath. Two fundamental experiments have been 
repeated again and again which would suffice to demonstrate, as F. 
5. Lee has so well expressed it, that the problem of ventilation is not 
chemical but physical—not respiratory, but cutaneous. These are: 
First, that subjects immured in close chambers and exposed to heat 
as well as the chemical products formed therein are not at all relieved 
by breathing pure outdoor air through a tube; and second, that 
they are completely relieved by keeping the chamber artificially cool 
without changing the air at all, and are relieved to a considerable 
extent by the mere cooling effects of an electric fan. 

Investigations made by the New York State Commission on Ventila- 
tion have shown that the temperature and the pulse-rate of an 
individual are markedly increased by even a slight increase in the 
room temperature; they also confirm Leonard Hill’s observations that 
overheated rooms enhance the susceptibility to respiratory diseases 
owing to changes in the mucous membrane which follow exposure to 


1 Science, N. 8., 1915, 41, 625. 


TECHNIC OF TREATMENT 699 


hot and dry air, and the resistance of animals to artificial infection is 
very definitely lowered by chill following exposure to a hot atmosphere. 

In connection with tuberculosis, in which the appetite is of such 
great importance, it is of interest that stagnant air reduces the desire 
for food perceptibly. In two series of experiments made by the 
above-mentioned Commission, standard luncheons were served to 
the subjects in the experimental chambers and the amount on their 
plates weighed. In one series the subjects consumed on the stagnant 
days an average of 1151 calories and on the fresh-air days an average 
of 1308 calories, an increase of 13 per cent. In a second series during 
colder weather, the average consumption was larger, 1492 calories 
for the stagnant and 1620 calories for the fresh-air days. 

We have here an explanation for the utility of fresh air in the treat- 
ment of tuberculosis. Stagnant air is bad primarily because of its high 
temperature and lack of cooling air movement, sometimes combined 
with high humidity. In fact, a lack of humidity, as Phelps has pointed 
out, makes hot air feel cooler and cold air feel warmer. It is very 
important that the air in a living room should not be dry, as it is in 
most of our artificially heated rooms during the winter. Living in 
stagnant air the patient feels uncomfortable, inert and listless, and 
above all, loses his appetite for food, which is very essential in the 
treatment of phthisis. The open-air treatment seeks to remove the 
drawbacks of indoor life amid stagnant air. For a certain, but limited 
number of patients it is attained best in a good sanatorium, but it 
may be just as well attained at home within the city ines in most 
houses. 

Technic of Treatment.—If the patient lives in a capacious home, or 
in one in which he may have a fair-sized, well-lighted, and ventilated 
room to himself, in a district or street which is not overcrowded, he 
may remain where he is. But in case he lives in the slum district of 
a large city, in a dingy and overcrowded tenement, he must move to 
better quarters which are available in every city. If his occupation, 
or that of those he depends on, is not in the way, it is even better that 
he move to the outskirts of the city, or to a suburb where certain 
advantages may be obtained which are not available or feasible in the 
city. 

A few words should be said about the various shacks, tents, special 
window tents, etc., which have been contrived for the city dweller 
with a view of giving him an opportunity to live outdoors, or in a well- 
ventilated room. Most of them are not feasible. They cannot be 
used in the thickly inhabited parts of cities; the tents or shacks can- 
not be placed in the back yards, on the roofs, ete., without attracting 
the curious, or even exposing the patient to eviction because of the 
resentment of the neighbors. I have seen a few patients in New York 
City who have made use of these contrivances, but they were rare 
exceptions, and they lived in private dwellings in the outskirts of the 
city. 


700 '  OPEN-AIR TREATMENT 


But the average bedroom, excepting in the dingy tenements, is 
sufficient for our purposes. If the patient is allowed to remove the 
window sashes, both the upper and the lower, as Cummings suggested, 
he may convert it into open-air sleeping quarters. The patient’s 
room should be large; one with a capacity of 3000 to 3500 cubic feet 
of air is best. But it must always be remembered that cubic space is 
of little value per se unless it is provided with efficient means of ventilation. 

In modern apartments, rooms with windows opening into air shafts, 
or narrow courts, are not good for tuberculous patients; they should 
have rooms with windows opening into the street, or a spacious court- 
yard. In apartment houses with elevators the top floor is the best, 
the higher the building the better. But in houses without elevators 
the advantages of the pure air in the upper stories are often negated 
by the exertion necessary in stair climbing by walking patients; but 
the ground floor should be avoided in tenements because it is 
almost invariably dark and badly ventilated. It should also be seen 
that trees do not obstruct the entry of air and light to the room, and 
favor excessive humidity. The windows of the room must be located 
so that the sun’s rays enter them for at least part of the day and pene- 
trate at least ten feet into the room. 

The walls of the room should be painted, not papered. All unneces- 
sary curtains and hangings should be discarded, leaving nothing but 
roller shades on the windows. Carpets are obviously bad, but some 
rugs should be left on the floor. Bare floors are apt to discourage the 
patient as well as those around him ‘The rugs can be taken out at 
frequent intervals, aired, and disinfected. The floor should be waxed 
or painted, so as to be easily cleaned. Steam or hot-water heating is 
best; gas heating is to be avoided because it consumes oxygen from 
the air. The usual contrivances to prevent excessive dryness of the 
air should be used. 

Afebrile patients who are allowed outdoor exercises should remain 
‘in the room very little during the day. In the city afebrile patients 
may leave their rooms soon after breakfast and go to some neighboring 
park where they are to spend the greater part of the day. In the out- 
skirts of the city, or in the suburbs, there may be sufficient space around 
the house, as well as porches, balconies, etc., on which they may exer- 
cise and rest comfortably, read, or do some light work under careful 
supervision of the physician. Intelligent patients may be given 
thermometers with directions to guide them as to the effects of exercise 
or work. Constant use of the thermometer by the patient is, however, 
a double-edged sword, as has been pointed out elsewhere. 

The season of the year has little effect on the outdoor life. The 
patient is to spend the greater part of the day outdoors during the 
winter, as well as during the summer. Only intense cold, or sun rays, 
rain, or strong winds, are to be avoided by seeking shelter. Excepting 
during blizzards, snow is rather invigorating to the average patient 
of this class. But here again it is to be borne in mind that very 


TECHNIC OF TREATMENT 701 


emaciated and anemic patients, also those over forty years of age, 
do not tolerate cold. 

Sleeping Porches.—Those living in the outskirts of the city or the 
suburbs may have tents in which they sleep during the night, and seek 
shelter during inclemencies of the weather. But the usual tent is 
rather stuffy and damp during the summer and autumn, and too cold 
during the winter for a tuberculous patient. There are made at 
present tent houses, or canvas bungalows, which are excellent because 
of the comforts they afford and the good ventilation that may be had 
within them. 





Fic. 117.—A knitted helmet for protecting head, neck and shoulders. (T.S. Carrington.) 


It is, however, best that the patient remain the greater part of the 
day on the porch and, in most cases, he may sleep in a bed placed on 
the porch. During the day, in case perfect rest is to be enjoined, he 
may remain on some form of reclining chair of which there are at present 
many on the market, such as the Universal Reclining Chair, the 
Kalamazoo Chair, the common hammock chair, the willow long chair, 
ete. During the cold winter, if he is not extremely anemic and emaci- 
ated and not over forty years of age, the patient may also remain on the 
porch on one of these chairs during the day, and in a bed during the 
night. “The whole problem is one of sufficient bedclothes and the use 
of some sort of hood or head covering (Fig. 117); in short, to dress 
especially for sleeping out.’’ As Cummings suggests, “by putting on 
a suit of underwear, a flannel shirt, pajamas of outing flannel, and a 
hood of flannel or eiderdown, and furnishing the bed with plenty of 
light weight but warm blankets and comfortables one can sleep with a 


702 OPEN-AIR TREATMENT 


continuous flood of fresh air in severe weather with perfect comfort 
and safety.”’ But it must be emphasized that the number of patients 
benefited by sleeping outdoors during the winter months is rather 
limited. Individualization is imperative. 

It is self-evident that sleeping porches are only feasible in rural 
districts, and not in large cities, excepting in their outskirts. But it is 
always important to remember that the proper construction of a sleep- 


OPEN 







SLEEPING 
PORCH 


OPEN 
NiadO 


BED ROOM 


SCALE 14"=1' 


Fic. 118.—Porch exposed on three sides; no provision for keeping the bed warm 
during the day. (MacWhinnie.) 


ing porch is not a simp’e matter. A. Morgan MacWhinnie! investi- 
gated 100 sleeping porches in the Northwest and found the follow- 
ing conditions: In 96 cases the sides of the sleeping baleony were 
partially protected from the wind and rain by a tarpaulin or some 
other material. Two had no protection whatever, and one was 
inclosed with glass windows which could be thrown open horizontally 


1 New York Med. Jour., 1914, 99, 780. 


TECHNIC OF TREATMENT 703 


at night on retiring. This was the only one that could be closed in 
the iy time, and had hot-water radiators connecting with the boiler 
in the cellar that kept the bed and its coverings as warm all day as the 
rest of the house. In 98 cases the bed, mattresses, linen, and covers 
were exposed all day to the dampness of the atmosphere. I found 
similar conditions in most of the sleeping porches in the East. 

The warming of the bedding and coverings and keeping them dry are 
elements which are very often neglected in open-air treatment, and 
it is not surprising that most patients cannot sleep outdoors on cold 


OPEN WEST 
= m~ 
8 ROOF = 
i if 
Oo. pats 
Oo a re) 
LJ 
faa) 
We 5 A 
CLOSED | a LUT TTT] 
i 3 
= 
a 
ea 
O 
x 
g 
= WARM ROOM 


” y 
SCALE % =1 


Fia. 119.—Ideal sleeping porch. When the bed is fully extended on the porch, the 
footboard closes the room from the outside air; when bed is in warm room, headboard 
closes opening to sleeping porch. (MacWhinnie.) 


and moist days. Moreover, an attendant must be engaged to attend 
to these details, and this is costly for the average patient. MacWhinnie 
suggested sleeping porches which have none of these disadvantages; 
they are so arranged as to be completely protected from the weather. 
He urges that the doors should be large so that the bed can be kept in 
the heated room during the entire day and bedding remains warm and 
dry. When ready for the night, it should be wheeled to the sleeping 
porch, thus obviating disadvantageous conditions mentioned above. 

Figs. 118 and 119 show the plan of a sleeping porch, designed and 
constructed by Dr. D. C. Hall. An opening is made in the wall large 


704 OPEN-AIR TREATMENT 


enough for the bed to roll through to the porch. The head and foot 
boards are so constructed that the opening in the wall is entirely 
closed when the bed is at full length on the porch or in the room. 
The room is thus kept warm for dressing in the morning. ‘The bed 
is supported by four large roller-bearing wheels, one hand of a child 
sufficing to move it out or in. Grips are so arranged that the bed can 
be drawn out or in, while the occupant is in the reclining position. 

The afebrile patient may indulge in driving, automobiling, or sleigh- 
ing during the winter, but always within the limits set by the physician. 

He should discard many of the pleasures of healthy people, even 
when he thinks he is well; he should not visit theatres, balls, crowded 
restaurants, ete., where large numbers of persons congregate and 
contaminate the air. Many a patient who has been doing well, and 
on the road to recovery, has suffered a relapse, or a complication, 
after attending a function at which a large number of persons got 
together in a confined space. Many suffer relapse, or reactivation 
of the disease after exposure to the vicissitudes of the weather. 

Open-air Treatment of Febrile Patients.— With febrile cases things are 
not so simple. They must remain in bed as long as the fever lasts, 
excepting under circumstances which are discussed elsewhere. In the 
city, the bed can only be kept within the room, and for this reason, as 
well as for others, it must be placed near the window, so that not only 
pure, fresh air may be avilable at all times, but also because the patient 
is usually encouraged looking out at the living world. In the suburbs 
the bed may be placed on the porch during the day during the summer 
months, and under certain circumstances it may remain there all the 
time. When feasible, a proper tent or porch is even better. Placing 
tents on roofs of houses in the city, or modifying fire escapes so that 
the patient may be kept on them in the open air, is not feasible. No 
patient wishes to expose himself to the curious gaze and commiseration. 
of the other inhabitants of the house, as was already mentioned. 

The good effects of the open-air treatment are often very striking in 
febrile cases. The general condition of the patient improves, a feeling 
of well-being ensues, replacing the despondency into which he was 
sinking. His strength returns. The anorexia and indigestion which 
sapped his strength disappear, or are ameliorated, and he eats with a 
better appetite. The painful cough often disappears within a few 
days and nights with open windows, or on the porch. This is at times 
the most salutary phenomenon; sometimes when sedatives have failed 
to control the cough, outdoor life works in this direction and the effect 
on the morale of the patient is marvellous. 

During the night open-air treatment is even more simple than 
during the day. It consists in one principle—open windows. There 
is no room in a decent house which cannot be properly ventilated by 
opening the windows, excepting during some of the hot and humid 
summer months in certain regions. But then the conditions outdoors 
are not much superior, and a tuberculous patient should not remain 





ABUSES OF OPEN-AIR TREATMENT 705 


during the hot and humid summer months in his home. If he cannot 
be moved, an electric fan will renew the air in the room properly. 

When dealing with young and plethoric individuals, and those who 
have been adapted to open air life, the windows may be opened com- 
pletely; the upper half may be lowered, and the opening should not be 
obstructed by any shade or curtain. But during the winter heat must 
be supplied in all cases, though the windows may be lowered after the 
patient has been properly covered. A sufficient number of woolen 
blankets, and plenty of flannel underwear, should be available for use, 
as required according to the temperature. There are people who can 
dress and undress in cold rooms, but they are rare; and tuberculous 
patients, especially those who are anemic and cachectic, cannot stand 
cold with impunity. But proper ventilation may be maintained in a 
room which is properly heated. 

Abuses of Open-air Treatment.—In an effort to get away from the 
stuffy wards and rooms in which tuberculous patients were formerly 
kept, we have recently gone to the other extreme and attempted to 
subject all patients indiscriminately to the open air treatment during 
all seasons. But it has been observed that a large proportion is not fit 
to live outdoors during the winter months. There are many healthy, as 
well as tuberculous, whose constitutions, or even habits which have been 
theirs since birth, are not adapted to cold air, and they, at times, 
suffer severely when persisting in carrying out the treatment as out- 
lined above. I have seen many patients distinctly harmed by life in 
a cold atmosphere. There are persons in whom cold induces catarrhal 
conditions of the respiratory passages, and even of the intestines; 
indiscreet exposure to cold is at times responsible for pleurisy, broncho- 
pneumonia, etc. Insomnia in the tuberculous is also very often the 
result of living ina cold room. Healthy persons are often kept awake 
in cold bedrooms. It has been found that in moderate climates, 
tuberculous patients feel better during the winter. But vital statistics 
show clearly that the mortality from this disease is highest during the 
winter and spring months, indicating that complications are more 
likely to arise during the cold months. ‘There is no doubt that compli- 
‘ating bronchopneumonia, pleurisy, and certain forms of bronchitis, 
which are common in tuberculous patients during the cold months, 
and which are often the last straw, could be prevented in many cases 
by avoiding exposure to cold. 

Open air treatment has also been abused while attempting to 
“harden” tuberculous patients. In many children the process of 
hardening, cold baths, frictions, and exercises, are beneficial. But in 
adults it is just as often harmful, especially when they suffer from 
tuberculosis. As has recently been pointed out by Kohler,' open air 
life is beneficial because it stimulates the production of heat in the 
body during the reaction which it induces; but these benefits are 


1 Ztschr. f. Tuberkulose, 1920, 31, 321. 
45 


706 OPEN-AIR TREATMENT 


observed mainly in persons before the period of katastasis, 7. e., before 
thirty-five years of age. Katastasis occurs in most tuberculous 
patients much earlier than thirty-five years, and for this reason it is 
dangerous for many of them to persist in living in a cold atmosphere. 
While pure air is usually cool, it must not necessarily be intensely cold; 
and renewing the air in a room should not involve the production of 
draughts. 

To keep an anemic and cachectic tuberculous patient comfortable, 
heat must be applied, especially to the extremities. Nearly all 
tuberculous patients over forty years of age, and a large proportion 
of younger ones, are safer in a warm, but well-ventilated home during 
the cold or chilly months of the year. All tuberculous patients should 
be properly clothed according to the season, and woolen underwear is 
imperative during the winter in most cases. Cold baths, taken in cold 
rooms, are decidedly dangerous for tuberculous patients, and for this 
reason it is, at times, impossible to find proper accommodations for them 
in the country during the winter. I have been convinced that many 
patients have been harmed while attempting to live in the country 
during the winter in houses and shacks which were not properly 
heated. In their homes in the city they can easily have pure and 
circulating air which is cool, but not cold. Of course, many patients 
have been “hardened” in this regard, but a large proportion succumb 
during the process. 

While attempting to ventilate sick rooms during the winter, draughts 
are to be avoided for the above mentioned reasons. Sudden changes 
in the temperature of the room should be prevented unless the patient 
is well covered. When leaving a warm room into the open air, appro- 
priate clothing is to be worn; many patients begin to cough soon after 
they emerge into cold air. Driving in open vehicles during cold and 
windy days should not be indulged in by tuberculous patients. Many 
complications, especially pleurisy, bronchitis, and catarrhal enteritis, 
may thus be prevented. 

It has been the universal experience that when the summer heat 
is accompanied by excessive humidity, tuberculous patients suffer 
from anorexia, insomnia, general weakness, etc., and they often lose 
the greater part of their gains during the winter. For this reason I 
insist that all patients under home treatment should leave for at least 
July and August for the mountains. But during the winter the 
majority of tuberculous patients are better off in the city, unless they 
are kept in the country in houses or institutions which are properly 
heated. 

Results Attained by Open-air Treatment.— The results attained by 
the open-air treatment depend on many conditions, notably the acute- 
ness and the stage of the disease. In acute, progressive cases we cannot 
expect much more than from any other method of treatment, except- 
ing perhaps more comfort to the patient than would be the case if 
he were kept indoors. The ultimate prognosis is gloomy at all events. 


CONTRAINDICATIONS 707 


In subacute cases the process is at times arrested and the disease then 
pursues the course of chronic phthisis. 

The good effects of the open-air treatment are best seen in the 
average case of incipient chronic phthisis which begins with moderate 
fever, nightsweats, anorexia, cough, etc. In advanced cases of the 
disease, when the patient is emaciated and apparently hopeless, several 
days of life in the open air often transform a despondent individual 
into one who shows his confidence in ultimate recovery very clearly. 
He gains in courage and is imbued with a desire for recovery; his fever 
declines, the nightsweats disappear, the cough and expectoration 
diminish, and he becomes hopeful in general. 

In the far-advanced stages of the disease the open-air treatment 
may only render the last days of life somewhat more bearable, contrib- 
ute to the false optimism which is often seen in these patients, and 
accentuate the euphoria which has been considered characteristic of 
the disease. But it is undoubtedly curative in the vast majority of 
incipient cases. The entire aspect of the patient is often transformed 
within a week or two, and the improvement is usually progressive. 
A good appetite with proper assimilation and digestion of the food, dis- 
appearance of the fever, nightsweats, insomnia, and amelioration of the 
cough, are the rule in these cases. Often it will be noted that fever, 
which resisted all other treatment for months, disappears after several 
days of life with open windows during day and night. Many patients 
learn it by experience and cannot be induced to close the windows. 
They have found that with open windows they sleep better, and feel 
refreshed in the morning, while closed windows induce cough, night- 
sweats, Insomnia, listlessness, etc. 

Contraindications.—It must be emphasized that there are but few 
contraindications to the open-air treatment. Even hemoptysis, how- 
ever severe, should not induce us to close the windows of the room 
inhabited by a tuberculous patient. Nor should they be closed during 
any season, provided the room is properly heated, as was already 
mentioned. Only during the summer, when the external air is often 
hot and humid, and even open windows are not effective in producing 
a free circulation of the air within the room, this method is often futile. 
An electric fan may improve conditions somewhat, but it is best that 
patients who can afford it should leave the city for a milder or colder 
region. 

There are many patients who do not bear the open-air treatment 
very well during the winter months; in fact, in some it is distinctly 
harmful, and if an attempt is made to apply it, it must be done with 
great care and circumspection. Patients who suffer from diffuse 
bronchitis in addition to phthisis do not bear cold air very well and so- 
called “rheumatic pains” in the joints are often aggravated by sleeping 
in a cold room; also those in whom the heart has been profoundly 
affected by the tuberculous toxemia—the poor circulation results in 
acrocyanosis, cold extremities, etc.; dyspnea and the cough are decid- 


708 OPEN-AIR TREATMENT 


edly provoked by winds, draughts, and cold air in general. ‘Those 
suffering from profound anemia at times cannot be kept warm by any 
means in a cold room. The same is true of old persons with bad 
peripheral circulation and extremely cachectic patients—they cannot 
be kept comfortable in cold rooms during winter nights. 

In all these cases it is necessary to heat the room, but the windows 
should under no conditions be closed completely. 

Phototherapy.—The value of light, especially sunlight, as a thera- 
peutic agent in tuberculosis has been appreciated for centuries. 
Climatic resorts, extolling their therapeutic efficacy, almost invariably 
mention the number of sunny days in the regions they are located. 
More recently Rollier' has written considerably about the great success 
he has attained in the treatment of articular, osseous and glandular 
tuberculosis in children by exposing them to direct sunlight in a certain 
fashion. Numerous other authors report excellent results not only in 
tuberculosis of bones and joints, but also the pulmonary forms of the 
disease. 

We have shown elsewhere that in extrathoracic tuberculosis any 
harmless drug, or therapeutic procedure, will give good statistical 
results, because the vast majority of cases tend to recovery, as long as 
they are kept at rest and not harmed by irrational surgery and medica- 
tion. Likewise, when exposure to the rays of the sun is cautious, no harm 
results In most cases of incipient, mildly active, and even advance 
disease which shows tendencies to sclerosis of the lesion. The statis- 
tical results may even appear excellent because of the salutary psychic 
effect, the patient feeling that something is being done for him. But 
when sunbaths, and other modes of application of direct sunlight are 
attempted in active and progressive pulmonary tuberculosis, and in 
laryngeal disease with especially contrived mirrors, the results obtained 
are not very striking. Indeed, when practised indiscriminately, 
deleterious effects are observed: Superficial burns, and even focal 
reactions in the lungs, eontributing to extension of the tuberculous 
process, may occur. 

More recently “artificial sunlight” has been lauded, especially by the 
manufacturers of certain lamps which have been urged on the profes- 
sion, and incidentally to tuberculous patients, at an exorbitant price. 
Having obtained good results in the treatment of certain tuberculous 
skin lesions by the use of the carbon arc light, Finsen urged the violet 
and ultraviolet rays of the spectrum as a therapeutic agent in treatment 
of pulmonary tuberculosis. Later, however, the mercury quartz 
lamp, of which there are now several models on the market, displaced 
all others.2. This mercury quartz lamp consists of a quartz container 
supporting mercury In a vacuum through which an electric current is 


1 La cure de Soleil, Paris, 1914. 
2 For a very thorough review of the literature and therapeutic results of sunlight and 


artificial light in the treatment of tuberculosis, see Edgar Mayer, Am. Rev. of Tubercu- 
losis, 1921, 5, 75-158, 


PHOTOTHERAPY 709 


passed. It is noteworthy that this lamp does not produce anything 
comparable to sunlight; the heat rays are almost entirely lacking, while 
the violet and ultraviolet rays are excessive at the expense of all other 
rays. 

It appears that here also inactive tuberculous lesions in the lungs 
are said to be benefited by the application of these violet and ultra- 
violet rays. Some have reported good results in cases of intestinal 
ulceration complicating pulmonary tuberculosis, but others have failed 
to obtain them. The same may be said about the application of these 
rays in laryngeal tuberculosis. From Mayer’s digest of the literature, 
and his own experience, it appears that in active and progressive 
tuberculosis, the quartz lamp has not shown any value as a curative 
agent. When applied with caution, there is one thing in its favor— 
it is a harmless mode of treatment. But when abused, it may cause 
headache, insomnia, tachycardia, and reactivation of the tuberculous 
process in the lungs, with their concomitant symptoms and results. 
Burns of various degress are not uncommon when the quartz lamp is 
recklessly applied, and at times large blebs result from over exposure 
of persons with delicate skin. However, from personal experience, 
as well from the reports of even overenthusiastic advocates, it appears 
that phototherapy can hardly be credited with any therapeutic value 
in tuberculosis in any of its forms. 

The same may be said of the treatment of this disease with the 
roentgen rays. Many authors, notably Bacmeister, Kupferle, De la 
Camp, and others, have reported good results when these rays are 
properly and cautiously applied according to a certain technic which 
they have worked out. But when we find here also that only afebrile 
and inactive cases are benefited, our suspicions are aroused that when 
used in small doses they may exert a favorable influence because the 
patient feels that something is being done for him; when used in large 
doses, by those who have not mastered the technic of roentgen therapy, 
harm may result of even greater magnitude than that lurking in 
phototherapy. 


GHA PT ERX XV 


CLIMATIC TREATMENT, 


We have seen that the vast majority of tuberculous patients are 
amenable to home treatment; if they are to recover at all, they can 
accomplish it without leaving their home surroundings. The autopsy 
findings showing that many persons have healed tuberculous lesions 
in the lungs and pleura, although they have never undergone a course 
of institutional or climatic treatment, prove clearly that tuberculosis 
is curable in all climates. But there are undoubtedly indications for 
certain forms of climatic treatment in tuberculosis, though they are 
not as imperative nor as necessary for the average case as the laity 
and part of the profession believe. In this chapter we shall attempt 
to review the indications and point out the limitations of climatic 
treatment. 

Climatic treatment of tuberculosis is probably older than any other 
method which has survived the recent advent of scientific medicine. 
The ancient Greek and Roman, as well as the medieval Arabic physi- 
clans were great believers in the efficacy of certain climates in the 
control and treatment of phthisis. The first thought that enters the 
mind of the average modern physician after diagnosticating a case of 
tuberculosis is, ““ Where should I send the patient’ If the physician 
is negligent in this regard, the patient will surely ask him, “Must I 
leave the city?” 

It is, however, a fact, agreed to by all entitled to an opinion, that 
recent studies of the effects of various climates on the incidence and the 
course of phthisis have not resulted in discovering a region on the habitable 
globe which can be relied on to cure or umprove all incipient or a sub- 
stantial proportion of advanced cases of the disease. Whenever geographi- 
cal, topographical, meteorological, and clinical data are correlated with 
demographic data for a given locality, and conclusions drawn that a 
very high percentage of cases recover while living there, there are at 
once shown other facts which prove conclusively that under climatic 
conditions diametrically opposed to these, the proportion of recoveries 
isabout the same. Jor these reasons many physicians have gone to the 
opposite extreme and claim that climate need not at all be considered as 
a therapeutic agent in the control and cure of phthisis. 

Economic Aspects of Climatic Treatment.—Other reasons militating 
against the extensive utilization of certain climates may be mentioned. 
Bearing in mind that the bulk of consumptives are recruited from the 
poorer strata of society and that even those who had been self-sup- 


COST OF CLIMATIC TREATMENT 711 


porting before they were attacked by the disease often become depend- 
ent soon after that event, it is evident that the economic factor is 
to be given great weight in this connection. Indeed, climatic treat- 
ment is as expensive as Institutional treatment; it is even more beyond 
the reach of most patients because modern municipalities provide, as 
a rule, institutions for the tuberculous, but hardly any supply funds 
with which patients may go to distant parts of the country and support 
themselves for a considerable time. 

This economic aspect of climatic treatment is too often disregarded 
by physicians who tell their patients, irrespective of their financial 
condition, to go to distant regions. Those who cannot raise the funds 
and must stay at home become despondent, and the prognosis is often 
aggravated as a result of it. Some of them go with meager funds to 
Colorado, Arizona, California, etc., and the result is even more dis- 
astrous. 

Cost of Climatic Treatment.—Thompson Fraser,! who has made a 
study of this problem in Asheville, N. C., and reported his observations 
in the Public Health Reports, shows that it must always be borne in 
mind that there is a clear relation between income and recovery in 
tuberculosis. When leaving for some climatic region, the patient 
must be prepared to provide himself with the proper requisites. If 
he lacks funds he should not undertake a trip which not only exhausts 
his resources, but does him no good; he should rather stay at home. 
He points out that at Asheville, and this holds good for nearly every 
other climatic resort in this country, the expense is about as follows: 

The cost of room and board varies within wide limits. From his 
observations at Asheville, board of fair quality with room costs from 
$10 to $12 a week at the houses which are licensed to take tuberculous 
patients. The price depends to some extent on the location of the 
rooms, the more desirable ones costing more, while less desirable rooms 
may be had for $8. The “extras,” Fraser points out, amount to 
almost as much as the cost of the room and board, including, as they 
do, additional food, milk, eggs, reclining chair, physicians’ fees, medi- 
cines, thermometers, blankets for cold weather, laundry, and every- 
ting that comes under the item of “incidentals.” 

Fraser’s conclusions are that the cost to the patient for a period 
of ten months, or forty-three weeks, at $8, $10, $12, a week would be 
$344, $430, $526, respectively, not including the extras just mentioned. 
A minimum of $700, therefore, exclusive of car fare, would be a more 
just estimate of the expense for the rather arbitrary period of ten 
months. These calculations were based on costs before the war. 
At present more than double the sums mentioned are necessary. 
If the patient is accompanied by some member of the family, it may be 
decided to keep house instead of to board, but this will not prove more 
economical in most cases. 


1 Public Health Reports, September 18, 1914, 29. 


712 CLIMATIC TREATMENT 


The estimate for room, board, and treatment for a period of ten 
months applies especially to those cases which can be benefited by a 
comparatively brief stay. If the disease has made greater inroads, 
and a longer stay is necessary to produce results, the cost of extras 
and perhaps of nursing may be prohibitive to the average consumptive, 
and it is wiser to remain at home where suitable food, care, and com- 
forts will more than outweigh the benefits of climatic factors, if un- 
assisted by these essentials. 

Climatic treatment is thus a luxury available for the chosen few, while 
the vast majority of sufferers from tuberculosis must perforce remain in 
their homes for treatment. 

Whenever I decide in favor of climatic treatment I inquire whether 
the patient has resources to hold out for at least one year. Under 
present conditions I insist that the expense will be at least thirty 
dollars a week. If he cannot raise that amount I discourage him from 
leaving the city. 

Effects of Change of Environment.—Looking with a sane and 
unbiased view on the problems of climatic treatment of phthisis, we 
find that it is undoubtedly an important adjuvant to our efforts at 
curing our patients. Even physicians who practice in cities, and have 
good results with home treatment are often impressed with the salu- 
tary effects of a change of surroundings. One has but to note the 
effects on a patient who has been kept at home for several months 
and all available hygienic, dietetic, and therapeutic measures to control 
the disease have been taken, yet the patient has been going steadily 
downward. A change in surroundings is decided upon, and he is sent 
out to the country, preferably a place the patient selects, provided 
there are no strong objections to it. It makes no difference whether 
the locality selected is at the sea coast or inland, in a forest or a desert, 
on a high altitude or the plains; it is immaterial whether the number 
of sunny days calculated by the weather man, or by the owner of the 
resort in the neighborhood, is small or large, whether it is foggy or 
even frequently rainy—the results are often astonishing. After 
remaining there for a few months, the patient returns greatly improved, 
in some cases even apparently cured. These are the facts which every 
observing physician is bound to meet in his daily practice and cannot 
be controverted by statistics or opinions of famous clinicians. But it 
is clear that in such cases it is not the meteorological or topographical 
conditions which are altogether responsible for the good results attained 
by the change. 

Carefully analyzing the results obtained by patients under my 
observation, I have arrived at the conclusion that the complex phe- 
nomena grouped under the title “change of environment,” or the 
psychic and biological response of the organism to a change in surround- 
ings, play here a greater réle than the difference in the composition and 
density of the air, or the number of sunny and foggy days. ‘The change 
in environment acts as a new stimulus, reinvigorates, and calls forth 
the dormant vital forces of the patient. 


EFFECTS OF CHANGE OF ENVIRONMENT W138 


Suggestion is a factor in climatic treatment of tuberculosis which 
has not been given the credit it deserves. The patient has heard that 
a consumptive cannot recover in the city, and, when unable to leave 
for any reason for some place reputed to be efficacious in this direction, 
he becomes despondent. Many brood over it to an extent as to 
nullify all other therapeutic measures. Once they are sent away, all 
potential and inherent vital forces are stimulated; despondency is 
replaced by a feeling of hopefulness, accompanied by an increase in the 
appetite, improved assimilation of food, diminution in the cough, ete. 
This is proven by the following facts which have come under our 
observation: 

Patients leave their homes where they have been under the tender 
care of relatives and have had good and properly prepared food, and go 
to the mountains or the sea coast where they are compelled to live in 
cheap boarding houses or hotels, in which the food given them is far 
inferior to that which they had been getting at home. Yet they thrive 
and gain in weight, while at home they had been wasting progressively. 
Others go to hotels and boarding houses which, for obvious reasons, 
allege in their advertisements that, in the reality much-coveted, con- 
sumptives are barred. In fear that when coughing the proprietor of 
the hostelry is liable to discover their ailment, the patients promptly 
cease coughing. In many cases the gain is only temporary, and after 
the so-called acclimatization, the “climate wears out.’ But the gain 
is immense in a large proportion of cases. The disease often takes a 
turn to the better, or the patient is carried over an acute exacerbation 
and given an opportunity to recover his inherent vital forces. 

This effect of a change of environment is often seen in patients, them- 
selves natives or residents of agricultural districts, even high mountain- 
ous regions, who have become sick with tuberculosis, and coming to 
the city to consult a physician improve, in spite of the fact that climatic 
conditions are undoubtedly inferior. But there has been a change of 
environment. 

That it is not entirely the climate per se which is responsible in all 
cases which improve by a change, is acknowledged by most authorities 
on medical climatology. Henry Sewall' points out an antagonism 
between the vital effects immediately attendant on a change of climate 
and those, often totally different in character, which may develop 
during permanent residence. “In short, a change of scene, irrespective 
of the character of the environment, has often temporarily a mysterious 
influence for good on the living organism. The first vital reactions 
to new climatic conditions involve especially the nervous system, the 
final effects are dependent on the modified metabolism of the individual 
organs, and this may or may not be conducive to the efficiency of 
the body as a whole.”’ Brown puts it pointedly when he says that 
without doubt many of the effects attributed to climate can be ascribed 
to change of climate. 


1 Klebs’ Tuberculosis, p. 664. 


714 CLIMATIC TREATMENT 


The writer has observed patients who left a favorable climate, where 
they have done badly, for an unfavorable one, where they soon improve 
wonderfully. Many immigrants who become tuberculous in New York 
City, try institutional treatment and fail to improve. A longing for 
their native land overtakes them, and they leave for home where they 
remain for some months and return to this country cured. We have 
observed numerous instances of this kind in New York. From personal 
observations, the writer can testify that the hygienic, sanitary, eco- 
nomic, and social conditions in southern Italy, Hungary, Russia, and 
Poland, where these patients go, are inferior to those in which they 
live in New York. Indeed, tuberculosis in those countries is more 
ravaging than here; is more often fatal. Nor are there sufficient 
accommodations for dependent consumptives. Still, many immigrant 
patients, who fail to get relief in the many excellent public sanato- 
riums in this country, in the mountainous regions of Colorado and 
Arizona, or the beautiful parts of Southern California, go to some large 
or small city in southern or eastern Europe and, after remaining there 
for several months, return apparently cured and able to work. 

There is no doubt that in such cases it is not the climatic conditions 
that helped, but the confidence they placed in their native lands, in 
the home surroundings, in the caressing tenderness of loving relatives, 
etc., which was instrumental in awakening the reparative forces of the 
organism. 

There are other reasons for sending patients, who can afford to go, 
to some region with a favorable climate. It is very often difficult to 
enjoin complete rest and freedom from the worries and anxieties of 
every-day life in the home of the patient. Nor can he be kept from the 
temptations of city life. ‘These objects may be accomplished by remoy- 
ing him from his home environment into some secluded country place. 
The patient is to be told that he will have to remain away from home 
for several months and he should not leave unless he has sufficient 
funds for the purpose. His relatives are to be warned against inform- 
ing the patient of any troubles at home. To this must be added the 
regular hours for meals, rest, exercise, etc., which are followed implicitly 
in the country, but often disregarded in the city with its temptations. 
I have had results which were astonishing with patients sent away in 
this manner. 

With some patients institutional treatment is best for these reasons, 
as will be shown later on, while with others the reverse is true. In 
fact, many patients are better off when sent out to roam freely in the 
country than when sent to closed institutions. 

Where to Send Patients.— Experience has shown that for the vast 
majority of cases of incipient and uncomplicated phthisis it makes little 
difference whether they go to a mountainous region or to lowland, to 
the sea coast or inland, to a moderate or cold region; the effect is 
practically the same, as long as they are taken away from their homes 
and placed under favorable surroundings, away from the troubles of 


MOUNTAIN CLIMATES 715 


home life. There is no climate which cures consumption, the many 
laudatory advertisements of institutions and railroad companies not- 
withstanding. The fact that nearly all successful sanatoriums, located 
as they have been in such a diversity of climatic environments, show 
practically the same proportion of cured, arrested, improved and last, 
but always least, dead, proves conclusively that if the climatic con- 
ditions are a factor, they are of least importance. 

A careful perusal of Guy Hinsdale’s prize essay on Atmospheric 
Air in Relation to Tuberculosis, which is one of the best books on the 
subject, and most impartial, because the author is not anxious to “‘boost”’ 
some region or institution, shows clearly that climate is of little thera- 
peutic importance in tuberculosis. He admits that good results are 
obtained in cloudy regions, as, for instance, in the Adirondacks, and 
at Rutland, Mass. He has no objection to sunshine, because the 
moral effects of bright sunny days, and plenty of them, are very great. 
As to the question of temperature and humidity, Hinsdale concludes 
that the majority of incipient cases do best in dry and cool places 
“not warm enough to be relaxing, but not so cold as to be repellant 
and restrict exercise and out-of-door life.’ The old ideas about 
equality of temperature, at least between the temperature of mid- 
day and midnight, are not of great importance; all mountainous sta- 
tions show great variations in this respect. Some variability tends to 
stimulate the vital activities, but in older people and those who are 
feeble, great variability is a disadvantage. Hinsdale denies that alti- 
tude per se has any great influence. It is of benefit mainly because it is 
incidentally associated with mountain life, with more sun, less moisture, 
and scattered population. One statement made by this author should 
be reprinted with heavy type in all discussions on the subject. “That 
a place is frequented by consumptives does not prove that it is a 
desirable place for them.” 

Mountain Climates.—When a change has been decided upon, the 
first thought which enters the mind of the patient, as well as that of 
the physician, is whether a high altitude is best. High climates have 
been popular for centuries; even ancient physicians, who believed that 
phthisis is invariably fatal, sent their patients to the mountains when 
feasible. Most of the modern sanatoriums are located in regions of 
more or less high altitude. 

We do not know why high climates are beneficial for consumptives. 
Various hypotheses have been formulated to explain it, but none have 
been proven. The purity of the air is beyond question; the absence 
of massed population assures freedom from air contamination. Humid- 
ity is also less frequent, though not so rare as some would lead us to 
believe, and many sanatoriums are located in regions which are notori- 
ous In this regard. The air is cool, even during the summer, especially 
in regions of 4000 feet or more above sea level. But the cold is not felt 
as acutely even during the winter owing to the greater diathermancy. 
The ozone, of which many writers of past generations spoke so much, 


716 CLIMATIC TREATMENT 


has been found to be worthless. There is very little ozone, and even 
if there were more we do not know that it would do much good to the 
patients. 

The diminished atmospheric pressure and rarified air have been con- 
sidered beneficial by increasing the mobility and expansibility of the 
thorax. It promotes deeper, fuller, and more frequent respiration. 
But how much of this is due to the outdoor life and whether outdoor 
life at lower altitudes has not a similar effect on consumptives, have 
never been satisfactorily investigated. 

The effects of high altitude on the hematopoietic organs and tissues 
have been investigated and some have found an increase in the amount 
of hemoglobin, others, a polycythemia, still others an increase in the 
number of leukocytes, etc. Webb and Williams! have found an 


increase in the lymphocytes, or mononuclear elements of the blood, as — 


an effect of high altitude. Some authors, notably Bartel, Bergel, 
Marie, and Fliessinger, have seen in this increased lymphocytosis in 
tuberculosis a defensive attempt on the part of these blood cells, while 
others see in it a demonstration that the lymphocytes contain a lipo- 
lytic ferment which destroys the waxy coat of the tubercle bacillus. 
Minnie E. Staines, T. L. James, and Carolyn Rosenberg? confirmed 
these findings in Colorado. They found that at an elevation of 6000 
feet the larger lymphocytes are absolutely increased in the circulating 
blood by at least 20 to 30 per cent in both man and monkeys. Webb, 
Gilbert, and Havens? found an increase in the blood platelets in tuber- 
culous human beings and monkeys, and that at higher altitudes the 
increase is even more pronounced. But that these blood platelets 
contain or supply opsonins, or that they play a réle in the cure of 
tuberculosis has not been proved. On the whole, it appears that 
the hematologic studies of phthisical subjects are contradictory and 
it has been shown that the conflicting findings have been due in a 
great measure to errors in technic. It may be stated that the hypoth- 
eses promulgated by some authors have not been confirmed by facts 
observed by other investigators. 

Some have maintained that the proliferation of connective tissue 
in the lungs, the true reparative process in phthisis, is enhanced by 
a residence in the mountains. But von Muralt, who formulated this 
theory, has not given any substantial and convincing proof. 

Even the statistics tending to show that deaths due to tuberculosis 
are less frequent in mountainous than in other climates have not with- 
stood scientific tests. It appears that tuberculosis was rare in the 
Rockies, the Andes, ete., so long as the population was sparse, the 
inhabitants leading an outdoor life, etc. But since cities have been 
established at high altitudes and social conditions favoring the develop- 
ment of phthisis created, the disease is not infrequent among the 

1 Tr. Nat. Assn. Study and Prevent. Tuberc., 1909, 5, 231. 


2 Arch. Int. Med., 1914, 14, 376. 
3 [bid., 1914, 14, 742. 


MOUNTAIN CLIMATES tle 


indigenous population. The American Indians, when infected with 
tubercle, succumb to the disease despite residence in the mountains. 

It is thus clear that economic and social conditions play the same 
role in the cure of tuberculosis in the mountains as they do in the 
plains or at the sea coast. On this point all authors are agreed. When 
a patient goes to a high chmate, penniless, and starves there, he will 
succumb just as quickly as he does in the slums of the city. If he works 
in Phenix, Denver, etc., while the disease vs active, he may breathe all 
the rarefied air, expand his chest to an extreme degree, and still succwmb 
just as quickly as in the city. It is only those who can afford rest, good 
nourishment, and careful medical supervision who are benefited by 
life in a high altitude, and most of these are also doing well in other 
climates. 

Indications for High Climates.—High climates are no panacea for 
tuberculosis; in some cases they are not an unmixed blessing. They 
have their indications and contraindications. 

Patients in whom a positive diagnosis of active phthisis cannot be 
made but who nevertheless show symptoms and signs of the disease— 
in other words, the so-called “ suspects’—may be sent to the mountains 
for a short or long stay on the principle that they need a rest anyway. 
But we must be careful and not suggest such a vacation to those 
with limited means. I have seen self-supporting artisans ruined, their 
children committed to asylums, while the father was sent away to 
the mountains without a positive diagnosis of tuberculosis. That 
they returned within a month or two reinvigorated and in excellent 
health was not sufficient to justify the sacrifice; the same result could 
have been obtained by less costly means. It is different with the 
well-to-do, who mostly court a vacation. 

A large number of neurotics, anemic and debilitated indinduals 
who are in constant fear of tuberculosis, and in whom a diagnosis has 
been made by some physician, but careful examination fails to elicit 
any symptoms and signs pointing to a lesion in the lung, are nearly 
always benefited by a stay in the mountains. Phthisiophobia, which may 
be considered a distinct syndrome common in modern times, should 
be treated in the mountains when patients can afford the change. 
They may remain under the impression that they have been cured of 
tuberculosis, but this does not make any material difference so long 
as they are relieved. 

Many of these “suspects” and “phthisiophobiacs”” may have been 
cases of abortive tuberculosis in which the physical signs were indefinite 
or absent. The rest in the mountains and the change of environ- 
ment undoubtedly contribute to their recovery. 

Incipient cases of tuberculosis with few constitutional symptoms 
gain considerably by a change for a mountainous climate. The appe- 
tite improves, the anemia vanishes, and they often gain in weight 
better than they would have in the city with its temptations. The 
patients are also freed from the troublesome solicitations of their 


718 CLIMATIC TREATMENT 


relatives and friends which are often more a detriment than a help to 
recovery. 

Active phthisis in the moderately advanced stage which does not improve 
under home treatment for any reason may be sent to the mountains for a 
prolonged stay. It is at times surprising to see marked improvement 
manifesting itself soon after their arrival in the country. Fever is no 
contraindication, provided it is not of the hectic or terminal variety, 
or due to some complication which may be aggravated in a high 
altitude. Occasionally a pleural effusion showing no tendency to absorp- 
tion will disappear after a stay in the mountains. F. L. Knight preferred 
patients of phlegmatic temperament to the nervous, with irritable 
heart, frequent pulse, and inability to resist cold. 

Of course, most tuberculous patients who can afford the expense 
should be sent to the country, preferably the mountains, during the 
hot and humid summer months. 

Contraindications.—As was already stated, high climates are like 
a double-edged sword and may be harmful. As a general rule it may 
be said that hopeless cases, running an acute course with hectic or high 
continuous fever, with a rapid extension of the process in the lungs, pro- 
found emaciation, edema of the extremities, etc., should not be sent, for 
obvious reasons. It is a great pity to send them travelling great dis- 
tances, which aggravates their already bad condition, to suffer or die 
among strangers. Their relatives are also to be considered. Upon 
hearing of the desperate condition of the patient on his arrival at his 
destination they may have to go to see him. 

Some of these progressive and apparently hopeless cases take a 
turn for the better with careful home treatment; the fever abates, the 
appetite improves, the strength begins to return. At this stage it 
may be well to send them away to the mountains where the improve- 
ment which began in the city is enhanced by the new surroundings. 
At any rate, they do not lose by the change and, when they can afford 
it, it may contribute greatly to their ult mate recovery. But they 
need experienced nurses to take care of them. 

Dyspnea is a strong contraindication to a mountainous climate. 
It is often not considered and the results are disastrous. Consumptives 
with dyspnea due to pulmonary emphysema, asthma, and fibroid 
phthisis, all of which mean cardiac dilatation; or due to cardiac hyper- 
trophy of a high grade, fatty degeneration of the heart muscle, nephritis, 
arteriosclerosis, etc., should not be sent to a high altitude. F. L. 
Knight objects to persons over fifty years of age. ‘Tachycardia, when 
the pulse is much over 100 per minute, and not slowing down after a 
long rest, is also a strong contraindication. 

Amyloid degeneration of visceral organs, advanced laryngeal, intestinal 
and peritoneal tuberculosis are contraindications. ‘This is not because 
the climate is harmful, but the hopelessness of the case precludes 
sending the patient far away from home. Schréder, whose experience 
has been very large, warns against sending patients with signs of com- 


SEA CLIMATES 719 


mencing cardiac weakness and with strongly accentuated neuroses to 
an altitude of over 1000 meters above sea level. 

In selecting a patient for a high altitude, we must not put very much 
weight on the climatic action on the pulmonary lesion; it is its influ- 
ence on the heart, bloodvessels, and nervous system that is important. 
If distinct disturbances in the structure or function of these organs 
are found, we must warn the patient against high climates. If there 
are strong reasons for sending him there, it must be done slowly— 
sending him first to a medium altitude and watching the effect, and 
when no harm is done he may be permitted to go higher, and finally, 
if he bears it well, he may go up as high as 6000 feet or more above sea 
level. It is obvious that these experiments can only be made with 
economically independent patients. 

It has been repeatedly stated that hemoptysis is more likely to 
occur in high altitudes than on the plains, but this is not substantiated 
by facts observed by physicians with extensive experience in the 
mountains. Available evidence tends to show that pulmonary hemor- 
rhages are no more frequent on mountains of moderate height (2000 to 
5000 feet) than in lower regions. Some authors, like Turban, state that 
they are even less frequent. 

The writer has sent to the mountains many patients with strong 
proclivities to bleed while in the city, and with the improvement in the 
general and local conditions, the tendencies to hemoptysis also dis- 
appeared. I have often been shocked by the advice given to patients 
who happen to get a hemorrhage while sojourning in the mountains, 
to leave at once, and they are in fact taken, while still bleeding, on a 
long journey. Moribund patients are thus brought to the city occa- 
sionally. 

Hemoptysis may occur in the mountains as well as in lower regions; 
it has not been proven that it occurs more frequently in the former 
places than in the latter. It seems, however, that the results of a 
copious hemorrhage may be more often serious in the mountains, 
especially in patients with impaired circulations, as has been shown 
by F. C. Smith.! His statistics show 56 deaths from pulmonary 
hemorrhages out of a total of 524 patients treated at the U.S. Public 
Health Sanatorium at Fort Stanton, New Mexico, with an altitude 
of 6231 feet. Ten per cent of deaths from pulmonary hemorrhages 
are not seen in other places. 

Sea Climates.—Ancient physicians recommended sea voyages for 
consumptives. English medical men of the first half of the nineteenth 
century considered long sea voyages indicated in many cases of tuber- 
culosis. The fact that they have recently been abandoned shows that 
they have not met with success. But we often meet with patients who 
want to take a trip around the world as soon as they are told that 
they are tuberculous. In other cases in which it is desirable to remove 


1 Tr. Nat. Assn. for Study and Prevent. Tuberce., 1908, 4, 246, 


720 CLIMATIC TREATMENT 


the patient from his home surroundings, the most feasible place is at 
the sea-coast. In fact, there are many cases in which, as we have 
just mentioned, high climates are contraindicated, and the patient, 
anxious for some decided change, asks whether a sea-coast resort is 
suitable for him. As was already emphasized, we must always consult 
the preference of the patient and send him to the place he chooses, 
unless there are strong reasons against it. 

It is obvious that the air on the high seas is pure and free from 
dust and microérganisms; but near the coast it is greatly influenced 
by the land climate, as well as by the industrial conditions in nearby 
cities. In fact, in some coast cities it is overloaded with dust and soot 
owing to mines, mills and factories in the neighborhood. 

But its moisture serves the purpose of equalizing the temperature; 
the seasonal differences are less pronounced. However, to this there 
are many exceptions, and before selecting a sea-coast resort, it is best 
to inquire carefully into the local meteorological conditions. 

According to Schréder,' sea air has a profound influence on the heart 
and bloodvessels. The cardiac activity is increased and the pulse 
slowed. He explains it by the action of the strong air currents and 
the greater heat conductivity of the moist air; despite the decrease 
in perspiration, the skin is better cooled and the bloodvessels contract. 
Reflexly, this causes a greater cardiac activity and the peripheral 
bloodvessels dilate, causing hyperemia of the skin. The result is 
strong circulation of the blood from the visceral organs to the periph- 
ery. The higher air-pressure causes slower but deeper respiration, 
favoring better metabolism and increased excretion of carbon dioxide. 
The activity of the skin, and especially of the mucous membranes, is 
greatly augmented. 

Sea voyages are not to be encouraged. “The siesstude of sea 
travel,’ says Guy Hinsdale, “the narrow cabins, and the difficulty 
of obtaining a suitable diet, even such common requisites as milk and 
eggs, should be enough to condemn sea voyages. ‘Tuberculous patients 
ought not to travel more than is absolutely necessary. Imagine the 
bacteriological condition of a consumptive’s stateroom, for instance, 
at the end of a month’s voyage. What sea captain or steward would 
ever put such a cabin into sanitary condition for the next passenger?” 
Then it must be borne in mind that sea sickness is liable to do much 
harm. I have seen many hopeful cases of tuberculosis take a bad turn 
after a sea voyage during which they suffered from sea sickness. 

As a therapeutic measure sea voyages are therefore to be condemned. 
But patients who are known to bear the travel well and who do not 
suffer from sea sickness may be permitted to cross the ocean when 
necessary. They are, however, to be warned against slow steamers; 
the sooner they get across, the better; and they must be told that it is 
best for them to spend the greater part of the time on deck and avoid 
the close cabin and the stuffy smoking-room. 


1 Brauer, Schréder and Blumenfeld’s Handbuch d. Tuberkulose, 1914, 2, 335. 


DESERT CLIMATES (21 


Empirically, it has been found that incipient cases without pro- 
nounced constitutional symptoms often do very well at the sea-coast, 
provided they observe the rules of healthful life. A slight tendency 
to hemoptysis is no contraindication, but those who show proclivities 
to copious hemorrhages, especially in the advanced stages, should 
avoid the sea-coast. Fibroid phthisis, as well as cases of tuberculosis 
with extensive pulmonary emphysema, are better off at the sea-coast 
than at the mountains, and I have seen cases relieved or improved, 
though in inland climates they had been doing badly. Similarly 
eases with cardiac and renal complications, which cannot be sent to 
high altitudes, should be sent to the sea-coast when a change is decided 
upon. Mild implication of the larynx is no contraindication. The 
cases of asthma and tuberculosis, in which dilatation of the heart is 
a strong feature, and which are not relieved, or are harmed, at a high 
altitude, should be sent to the sea-shore where they often recover their 
strength ina marvellous manner. ‘The same is true of senile consump- 
tives with rigid arteries and rigid chests, in whom paroxysmal attacks 
of cough and expectoration are occasionally very annoying. They are 
often benefited by a stay at the sea. Phthisis with chronic bronchitis 
in which the amount of expectoration is excessive, is relieved at times 
in a sea climate. Mild forms of neuroses and metabolic disturbances, 
such as gout, diabetes, obesity, etc., when complicated by tuberculosis, 
do well at the seashore. 

Of course, far advanced cases with hectic or high continuous fever, 
or with laryngeal, intestinal, and renal complications, as well as acute 
progressive cases, should not be sent to the sea-coast but should be 
kept at home. 

Desert Climates.—There yet remains to speak of desert climates 
in which many patients in this country have been cured by “roughing 
it.’ These regions may be of low or medium altitude. But their most 
important characteristic is the capriciousness of meteorological con- 
ditions; the changes are quick and extreme. The air is pure—there 
are usually not enough people to contaminate it—but it is frequently 
filled with dust and sand, especially after strong winds and storms. 
Of sunshine there is plenty, often to the detriment of the patient, who 
finds it hard to contrive a shelter against it. 

Because of the frequent changes in the weather, strong, often violent 
winds, these climates make very great demands upon the reactive 
powers of the patient, and lead to excessive expenditure of vital force. 
They are therefore suited only for those endowed with strong con- 
stitutions and who have ample recuperative powers. ‘The very young 
and the very old and those with delicate constitutions should not be 
sent to the desert. Moreover, patients of the class Just mentioned as 
proper cases for desert climate are not satisfied with climate alone. 
They demand, as a rule, also social life and amusements to distract 
them, and these they cannot get in those regions. 

It has been found empirically that patients with phthisis compl- 

46 


ee CLIMATIC TREATMENT 


cated by bronchitis and pulmonary emphysema, who expectorate exces- 
sively, often do well in these regions. Patients with phthisis compli- 
cated by renal disease may also do well, provided there is no arterio- 
sclerosis. Occasionally, we meet a patient in a far advanced stage of 
the disease who has been “given up,” but he decides to discard all 
comforts and pleasures of life and leaves for some desert region, and 
within a couple of years returns in excellent condition. These cases 
are rare, but they do occur. Unfortunately, they admit of no generali- 
zation. 

A Warning.—Before leaving the subject of climatic treatment of 
phthisis, I want to emphasize the fact that it is not only good air but 
also good residence and above all good food that the patient must 
have if he is to recover. These three in combination are very difficult 
to obtain. William Garrott Brown, an American historian, who suc- 
cumbed to phthisis after making a vain fight against the disease, thus 
describes his experiences: 

“Tt is now seven years and more since I began my quest for a place 
and an arrangement to breathe freely and constantly the right kind of 
air, and eat in abundance the right kind of food, yet I can say with 
perfect honesty that I have not yet found anywhere the combination 
of these two factors of cure worked out satisfactorily at moderate 
cost for me and such as | am.’ He points out that American cookery 
is peculiarly exasperating—‘ that is to say, the cooking of such Ameri- 
cans, doubtless the majority, as can be induced to ‘take boarders,’ 
and particularly such as can be induced to take boarders who are 
sick. Many of these last, by the way, are such as have already failed 
to minister acceptably to boarders who are well. There is, as a rule, 
not merely unenlightened American cookery; but cookery stimulated 
by no aspiration and but little competition; cookery seasoned with a 
lax indifference; cookery without any compelling need to be better, 
and with an obvious reason for being as careless and unlaborious as 
it can be and continue to be endured. To take ‘lungers’ at all, it 
would seem, confers rather than incurs an obligations. For is not that 
surrendering the chance of any other kind of gainful hospitality?” 

These are the reasons why many patients who have done well at 
home take a turn for the worse after a sojourn in the country for a 
few months. Physicians should bear this food problem in mind when 
sending their patients to boarding houses in the country, and when 
the place selected has an ideal climate but does not have the facilities 
for proper housing and feeding the patient, he is safer at home under 
a carefully regulated open-air treatment, as was already described. 


CHAPTER XXXIX. 
INSTITUTIONAL TREATMENT. 


Sanatoriums.—We have shown that success in the treatment of 
tuberculosis can only be attained by gaining the confidence and the 
cooperation of the patient and retaining them over a long period of 
time, until the termination of the case.. The old adage that rest, proper 
nourishment, and fresh air are effective as curative agents, holds 
good today for most cases. But they can only be of benefit when taken 
methodically, and adjusted to the special requirements of each indi- 
vidual case. The tuberculous patient is usually an individual who has 
not led an exemplary hygienic life, as is proven by the fact that the error 
of his ways has been instrumental in reducing his natural, and inherent, 
resisting forces against the ravages of the tubercle bacilli. He must, 
therefore, be guided into a healthful mode of life. He must also be 
eared for in such a manner as to preclude the dissemination of the 
seeds of the disease among those who come into contact with him. 

These are some of the reasons why there have recently been estab- 
lished institutions with a view of solving the complex prophylactic, 
therapeutic, and social problems of tuberculosis. In these “sanato- 
riums”’ the patients are under the constant supervision of especially 
trained physicians who scientifically and methodically guide them 
along climatic, dietetic, and specific lines of treatment. The rules of 
rational life are minutely enforced, and the discipline is of a military 
character in practically all well-conducted institutions. 

As soon as a diagnosis has been made, the problem is presented 
whether the patient should be sent to one of these sanatoriums, or 
may be cared for at home with an equal outlook for ultimate recovery. 
In deciding this question it is necessary to take into consideration 
many factors which are but rarely thought of. 

Scope of Sanatoriums.—The first sanatorium was established by 
George Bodington in 1840, as has already been mentioned (see p. 696). 
But he failed. Herman Brehmer established the first successful sana- 
torium in Germany in 1859, at a time when tuberculosis was considered 
incurable because of the teachings of Laennec, and the experience of 
ancient physicians. In this country Trudeau established the first 
sanatorium at Saranac Lake in 1884 and met with considerable suc- 
cess, discharging cured patients, a thing which was in those days 
considered impossible. With the evolution of our knowledge of the 
etiology, pathology, and therapy of the disease, the functions of the 
sanatorium have been greatly enhanced. It has been expected that it 


724 INSTITUTIONAL TREATMENT 


would prove of great prophylactic value by affording places for the 
segregation and isolation of the bacilli “carriers;” that it would prove 
of immense therapeutic value because it was assumed that modern 
methods of climatic, dietetic, and specific treatment can only be 
carried out under the careful supervision of especially trained physi- 
clans; that it would prove of great educational value, teaching the 
patients a healthful mode of life which is in itself an important weapon 
in the struggle against the disease, and which may be followed by 
them after their discharge from the institutions. 

With these aims in view, numerous institutions have been established 
in nearly every country of the civilized world at an outlay of immense 
sums of money for buildings, equipment, and maintenance. In some 
countries the State and private insurance companies have provided the 
funds for the sanatoriums. The fact that within recent years the 
mortality from tuberculosis has decreased was considered striking 
proof of the valuable results attained, and the sanatoriums have 
been given the lion’s share of the credit. 

But at present, after these institutions have been in existence for 
over thirty years, we hear inquiries from many competent sources 
whether they have done all, or the greater part, of what has been 
expected of them. Articles like that of Edward 8. McSweeny,! 
Medical Superintendent of the Sea View Hospital in New York, “Are 
We Getting Proper Value from Our Plant and Expenditure for the 
Tuberculous?” are becoming more and more frequent in our medical 
journals. T. D. Lister? is of the opinion that “too much is sometimes 
claimed as the result of the institutional training of patients.” Con- 
sidering that immense sums of money have been invested in these 
institutions, it is but proper to inquire whether they have brought 
returns along therapeutic and prophylactic lines commensurate with 
the investment. 

Limitations of the Usefulness of Sanatoriums.—It seems that the 
pessimism as to the value of sanatoriums displayed at present is 
mainly due to the fact that too much was expected from them. They 
are no panaceas for phthisis. Some enthusiasts, who have advocated 
their erection and raised funds for the purpose, have in fact promised 
too much, and when at present these institutions do not come up to the 
extravagant expectations of some, they are altogether condemned. 
This is as unjust as the extreme enthusiasm of those who claimed 
that sanatoriums will solve the tuberculosis problem. In an official 
report signed by Clifford Allbutt, Lauder Brunton, Arthur Latham, 
and William Osler,’ on the value of sanatorium treatment, it is stated: 
“In many cases, owing to the severity of the disease present, it must 
be useless; that in a few instances it Is actually harmful; and that in 
many cases this method of treatment need not be carried out in an 


1 Medical Record, 1915, 87, 94. 
2 Lancet, 1917, 2, 739. 
3 Thid., 180. 


SANATORIUMS #25 


institution.” Bardswell and Thompson’s! analysis of the experience 
of the King Edward VII Sanatorium at Midhurst leads to the following 
conclusion: ‘The records show that residence in a sanatorium, 
much though it can accomplish in individual cases, is a means of treat- 
ment which is far from being adequate.” 

Before pointing out the cases in which the sanatoriums may be 
utilized with benefit in the treatment of phthisis, we shall enumerate 
some of the shortcomings of this method of treatment: 

The number of sanatoriums is inadequate, and we cannot expect 
that there will ever be a sufficient number to provide for all tuber- 
culous patients, just as we cannot expect that all suffering from active 
disease can be induced to enter and stay within the institutions until 
the termination of the affliction. In the available institutions there 
is hardly place for 5 per cent of the existing proper cases. To provide 
accommodations for all suitable cases in the United States, several 
billions would have to be invested in buildings and equipment, and 
then at least $100,000,000 annually for maintenance. Even the most 
enthusiastic of those engaged in the campaign for the control of 
tuberculosis are not hopeful of ever raising such enormous funds. 

Sanatoriums are expensive, and it is problematical whether the 
results attained within them could not be achieved in the vast majority 
of cases at a lesser expenditure with home treatment. It costs at 
least $3.00 per day to maintain a patient ina sanatorium. The experi- 
ment has never been tried on a large scale to spend that much money 
on a large group of patients treated in their homes consistently for 
many months. . 

It appears that only the very rich or the very poor can afford insti- 
tutional treatment for months under present conditions. The former 
can pay any price, and the latter are cared for in enlightened cities 
by the State, municipal, or philanthropic institutions. But there is 
a large middle class which will only reluctantly agree to be treated as 
public charges, as is the case with clerks, small merchants, profes- 
sional persons, etc., who have been self-supporting until stricken by the 
disease. They cannot undertake to pay at least $30.00 a week for 
several months, and at the same time provide for those dependent on 
them. Neither are they inclined to enter State or municipal sana- 
toriums, and associate with persons who may be distasteful to them. 
Only when the disease has advanced far, often beyond repair, and all 
their own and their friends’ resources have been exhausted, do they 
decide to enter sanatoriums as a last resort, and even then they often 
leave soon after entering because the surroundings are distasteful to 
them. ‘This is the main reason why so few incipient cases, derived from 
these classes, are entering sanatoriums. 

It is very difficult to induce patients in the incipient stage of the 
disease to enter sanatoriums because they maintain that they feel quite 


1 Mortality after Sanatorium Treatment, Med. Research Committee, Special Report 
Series No. 33, London, 1919. 


726 INSTITUTIONAL TREATMENT 


well and resent the idea that they must live among “sick,” or among 
“consumptives,’’ and they often leave soon after entering for these 
reasons. The strict discipline, especially the unavoidable institutional 
atmosphere, is distasteful to the average human being who will resist 
all attempts to place him in an institution as long as he can. The policy 
of admitting only hopeful cases and discharging bed-ridden or dying 
patients, does not meet with the success worthy of the effort. 

Many patients refuse to enter sanatoriums because they do not 
want to have the stigma of tuberculosis which, they allege, will stick 
to them throughout their lives and may interfere with getting employ- 
ment under present conditions of private and municipal phthisiophobia. 

It can be stated without fear of meeting proofs to the contrary that, on 
the whole, sanatoriums do not show better lasting results than properly 
conducted home treatment. In this country, hardly any State or munici- 
pal sanatoriums have published satisfactory reports with comparative 
statistics showing the results attained as compared with a similar 
group of patients treated in their homes. The most competent com- 
pilations of statistics have been published by Lawrason Brown and 
Pope! about the discharged patients from Saranac Lake, and by 
Herbert Maxon King,? of the Loomis Sanatorium and by Bardswell 
and ‘Thompson on the experiences of the King Edward VII Sanatorium 
at Midhurst. To be sure, Brown shows that five, ten, and even 
eighteen years after discharge some of the patients were found alive, 
and even efficient at their occupations. But the average life of the 
consumptive outside of the institution, under any mode of treatment, 
has been founds to be between six or seven years. Stadler’ reports 
that five years after the onset of the disease one-half of tuberculous 
patients are found able to work without sanatorium treatment. There 
are sunilar statistics available for other countries, and I have no doubt 
that in the United States we would find conditions the same on careful 
investigation. King’s conclusion as to the value of sanatorium treat- 
ment is that his inquiry “clearly demonstrates the uncertainty of 
apparent immediate results of treatment.” 

This uncertainty refers mostly to relapses, which are to be expected 
when we consider the undulating course of phthisis, with its periods 
of remissions and of acute or subacute exacerbations. The few investi- 
gations that have been made of patients discharged from sanatoriums 
in New York show distinctly that a very high proportion have suffered 
from relapses of the disease, despite the fact that they have been found 
“apparently cured,” or “improved”’ at the time of their discharge. 
Many have to be readmitted because of these relapses, and it has been 
said that the cure is so good and attractive that many patients like 
to take it several times. 

It is clear that patients who die during, or soon after, sanatorium 


1 Am. Med., 1904, 8, 879; Ztschr. f. Tuberkulose, 1908, 12, 206. 
2 Tr. Nat. Assn. for Study and Prevent. Tuberc., 1912, 8, 82. 
3 Deut. Arch. f. klin. Med., 1902, 75, 412. 


SANATORIUMS 127 


treatment are to be deducted from the total number of patients when 
we want to arrive at an estimate as to the cost of each “cured” case. 
Dr. Taylor, Tuberculosis Officer, Country Borough of Halifax, reports 
on “The After Histories of Insured Persons Granted Sanatorium 
Benefit During 1914, with a Critical Review of the Facts.’! He 
remarks that of 1914 applicants treated, 76.5 per cent are dead, and of 
the remaining, 23.5 per cent half are unable to work. The County 
of London Committee records the discharge from sanatoriums in 1919 
of 1484 ex-service males, of 690 civilian males, and of 761 females. 
Of the first group 699, of the second, 294, of the third, 293 were unfit 
for work when discharged; 25, 27, and 23 died in the sanatorium. 
Midhurst reports that of the 1906-7 discharges 66.4 per cent were 
known to be dead by 1919. The percentage does not fall below 50 
until we reach the 1916-17 discharges, of whom 40.1 per cent were dead 
by 1919; while of the 184 discharges in 1917-18, 45 (25.4 per cent) 
were known to be dead, and 21 had been lost sight of. At Newcastle- 
on-I'yne of those discharged in 1913, 48.4 per cent were known to be 
dead in 1919, and 18.8 per cent had been lost sight of. Of discharges 
in 1917, 28.8 per cent were dead and 11.9 per cent had been lost sight of. 

In estimating the problem whether sanatoriums bring returns com- 
mensurate with the money invested in their erection and maintenance, 
we must also deduct those cases which suffer relapses, for obvious 
reasons. And when we do this, in addition to combining with them 
those who have been discharged because the sanatorium was of no 
benefit to them, and also those who died, we discover that the cost per 
successful case 1s enormous and hardly attractive to municipal and State 
authorities. 

The exorbitant cost of sanatoriums is shown in another way. It is 
well known that from 25 to over 50 per cent of the inmates in the 
institutions which aim at admitting but “incipient”’ cases are “closed”’ 
cases, with negative sputum. Some authors are inclined to estimate 
that over 50 per cent of these abacillary cases are in fact non-tubercu- 
lous. C.D. Partfit estimates conservatively that 33 per cent of the 
abacillary cases which are classified as moderately advanced cases of 
tuberculosis are non-tuberculous. It is on these cases that such large 
sums are spent with a view of preventing and curing tuberculosis; they 
improve the statistics of success of the institutions. When we con- 
template the cost we are astounded. I assisted at the autopsy on a 
woman who spent twenty-six years continuously in a sanatorium and 
a hospital for advanced consumptives. We found that she had no 
active tuberculous lesion. Even if we count only $500 per year, the 
community wasted $13,000 on this woman, in addition to the loss of 
her work which might have been more than this sum, if she had not been 
kept in an institution. Then, she kept out at least twenty-six patients 
who really needed hospital care. The sanatoriums and hospitals in 


1 British Med. Jour., 1920, 2, 216. 


728 INSTITUTIONAL TREATMENT 


this country all have numerous such cases. This is proved by the 
statistics of Ash and Washburn which we have already quoted (see p. 
534). 

The educational value of the sanatoriums is beyond question, teach- 
ing, as they do, objectively the rules of healthful life. But the patients 
of the lower social strata, who make up the bulk of dependent con- 
sumptives, cannot, as a rule, continue along the hygienic lines which 
they have learned. Returning to the tenements, with rooms without 
windows or baths, coupled with a low earning capacity, one cannot 
live in the manner he learned in an institution. Relapses, which are 
likely under all circumstances, are inevitable for these reasons alone. 
In England Dr. Lister and many others have considered the educational 
value of sanatoriums a great failure. 

On the other hand, the aggressive campaign, recently carried on by 
the various antituberculosis agencies has done all that can be done 
along educational lines. In fact, the dispensaries with their social 
services, the day and night camps, etc., achieve educational, as well 
as therapeutic results which are, from a certain viewpoint, superior 
to, and more far reaching, than those of the sanatoriums, and at less 
cost. 

Let us not overestimate the prophylactic value of the sanatoriums. 
It was hoped that by segregating consumptives, sources of infec- 
tion would be isolated. But we have already shown that this was a 
vain hope. Only “incipient” cases are admitted—so far as they can 
be found and induced to enter in time—while advanced cases, which 
are the most dangerous, because they expectorate myriads of tubercle 
bacilli, are rejected. The statement that institutional treatment is 
the predominant cause of the decline in the death-rates from phthisis, 
which has been expounded by Newsholme! with such vigor, is not 
supported by facts. Newsholme’s figures have been demolished by 
Karl Pearson,? one of the most competent authorities to judge statis- 
tics. In Germany—the home of the sanatorium—this claim has been 
abandoned during recent years. As was pointed out by Cornet and 
Robert Koch at the Antituberculosis Congress in London, there were 
at least 226,000 persons disseminating tubercle bacilli in Germany, 
and only 20,000 were cared for in institutions, and of these latter only 
4000 expectorated bacilli. This number could not have had any per- 
ceptible influence on the morbidity and mortality from tuberculosis. 
In the United States conditions are the same. In recent attempts at 
prophylaxis of transmissible diseases no attempts are made to isolate 
cases when the number of “carriers” is large. This point has been very 
well elaborated by one of the best sanitarians, Charles V. Chapin. 
Why tuberculosis is an exception has not been shown. Indeed, it has 
been aptly stated that it would be much easier to segregate those who 


1 Prevention of Tuberculosis, London, 1908. 
2 Fight against Tuberculosis and the Death Rate from Phthisis, London, 1911; Tuber- 
culosis, Heredity, and Environment, London, 1912. 


CAUSES OF FAILURE OF INSTITUTIONAL TREATMENT 729 


had not been infected with tubercle bacilli than those who harbor this 
virus in their bodies. The number of the former is much less. (See 
Chapter ITT.) 

From the clinical standpoint, we are not in possession of relvable 
statistics showing that the mortality of patients who have been treated 
in sanatoriums is lower than that of those who have been cared for in their 
homes. The statistics of experiences in English sanatoritums, quoted 
above, seem to show that it is as high as could be expected if no treat- 
ment had been instituted. We have already mentioned that the insti- 
tutions in the United States have not published comprehensive data 
along these lines, excepting those of Lawrason Brown and King. In 
Germany, although long and apparently learned books and articles 
have been produced, they are just as much in the dark about this 
problem as we are in this country. The reasons are that the material 
is not comparable. A drastic illustration may be cited. In the selec- 
tion of cases it is aimed at admitting only those in the incipient stage. 
The result is that at Grabowsee 45.2 per cent, and at Melsungen 97 
per cent of the patients have not shown any tubercle bacilli in the 
sputum. Ulrici reports that in 40 per cent of the patients at Mulrose 
he could not make a positive diagnosis of tuberculosis, and Leube says 
that many patients who are admitted to sanatoriums in Germany 
are, when examined by military surgeons, found fit for the army and 
accepted. And during the World War, the military authorities found 
that a large proportion of these consumptives made _ excellent 
soldiers. To be sure, the outdoor life and the regularity in habits 
which military service involves, as well as the nourishing food, may be 
some of the factors in improving many tuberculous patients, as some 
have suggested. But it seems to me that the greater number of these 
patients, though they had been in sanatoriums, were not at all tuber- 
culous. They are derived from the class collectively grouped as “‘ con- 
sumptives with negative sputum. 

It is obvious that statistics of such “consumptives” will show good 
and lasting results of treatment. In their book on the prognosis of 
tuberculosis Kuthy and Wolff-Eisner, reviewing the subject, say that 
exact and scientific data are not available to prove the value of sana- 
torium treatment; and Newsholme, who is a great believer in the 
benefits of institutional treatment, also says that there are no exact 
and comparable data available to prove it. 

Causes of Failure of Institutional Treatment from the Therapeutic 
Viewpoint.— While institutional treatment undoubtedly has its advan- 
tages, which will be shown later on, it is by no means the best, and 
clinicians cannot approve of all the methods pursued in sanatoriums. 
The fact is, wholesale treatment of such a complex disease as phthisis os 
not ideal. Individualization rs here of greater importance than in most 
other diseases. Says Albert Robin:' “One of the disadvantages of 


1 Traitement de la tuberculose, Paris, 1912, p. 67. 


730 INSTITUTIONAL TREATMENT 


the sanatorium is that it applies too often arbitrary principles to 
patients whose disease can only be relieved by individualized methods. 
It is for this reason that the practitioner who knows how to adapt 
the treatment to each of the small number of patients under his care, 
and to take cognizance of the temperamental indications, is qualified 
to manage a case of tuberculosis as well as, if not better than, the 
sanatorium doctor who has under his care a large number of patients 
of whose individual idiosyncrasies he is ignorant, at least for a time, 
and must therefore have a strong tendency to subject them all to the 
same method of treatment.’’ This refers to private sanatoriums, In 
which the patients must be catered to if they are to be retained for 
months. In State and municipal sanatoriums, where the poor and 
dependent patient faces starvation if he leaves the institution, the 
trouble is of a diametrically opposite character. The fact that a large 
proportion of patients leave before the physicians consider them fit 
for discharge, shows that they cannot be satisfied. 

This lack of individualization in treatment is seen In many ways in 
the sanatoriums which are hotbeds of therapeutic hobbies. But this 
is usually not so harmful as the uniformity of the diet in institutions. 
Mass feeding is difficult at best and can only be carried out in jails, 
where the inmates have no choice, or in armies during war. In a discus- 
sion on the sanatorium problem in England, T. D. Lister! thus sum- 
marized the food question: “It is badly cooked, badly served, from 
ignorance or lack of sympathy for human weaknesses, from unneces- 
sary monotony in the daily menu. For the convenience of the staff and 
store room there is a melancholy recurrence of the same food after the 
same intervals in some sanatoriums. Loss of interest and loss of 
appetite result. Patients, staff, and doctors often become institu- 
tionalized. ‘There is always a risk of deterioration in official clinicians.” 
To subject to the same dietary tuberculous patients in different stages 
of the disease, with different individual capacities for digestion and 
assimilation, who have been brought up on, and adapted to different 
kinds and preparations of foods, is bound to meet with failure. For 
this reason we find that complaints about the quantity and quality of 
the food are universal in public sanatoriums, and to some extent in 
private institutions where food is served & la carte. 

It can hardly be expected that municipal, State, and philanthropic 
sanatoriums should supply food @ la carte; it will always be table 
dhéte. And for this reason resentment on the part of the patients 
is to be expected. To be sure, these institutions are always filled and 
there are long waiting lists, though during recent years the latter seem 
not to be such a striking fact as it was formerly. But when patients 
leave before they are discharged, we may safely assume that the cost 
incurred during several weeks or months for their maintenance was, to a 
large extent, wasted. 


1 Lancet, 1917, 2, 739. 


INDICATIONS FOR INSTITUTIONAL TREATMENT 731 


In American municipal sanatoriums of the large industrial cities 
the failure in this regard is even greater than in other countries, 
because we must care for tuberculous immigrants of various nation- 
alities, whose tastes differ extremely as regards food and its preparation, 
as is shown elsewhere in this book. 

These are some of the drawbacks of sanatorium treatment. It is 
for these reasons that the municipal and State sanatoriums in many 
cities of the United States are not filled with a desirable element, but 
contain a large proportion of undeserving individuals. “My efforts 
are not going to be devoted to coddling tramps and other parasites,”’ 
exclaims in despair Dr. Edward S. McSweeny, the Medical Superin- 
tendent of the Sea View Hospital in New York. These are also the 
reasons why the best elements of the tuberculous population in this 
country will always have to be cared for in their homes, as is the case 
at present. 

Indications for Institutional Treatment.— But there are many cases 
of tuberculosis which cannot be treated in any other place than in insti- 
tutions. In fact, anyone with experience in a large city is convinced 
that tuberculosis cannot be managed without the aid of institutional 
treatment. Of the cases which are suitable for sanatorium treatment 
and would be lost without it, we may mention the following: 

Among well-to-do patients we meet with many who, for various 
reasons, cannot be cared for in their homes. To send them to the 
country without control may prove disastrous, because the foolish 
and reckless rich show at times greater lack of self-restraint than the 
stupid poor. They are best cared for in private sanatoriums in which 
most of the drawbacks of the public institutions are eliminated. They 
may be sent to sanatoriums for a short stay, over the hot summer 
months, or for outdoor treatment for the relief of an acute exacerba- 
tion, ete.; or for a long period till the disease is arrested. Great care 
should be taken that they do not become egocentric, excessively 
introspective, or hypochrondriacs, which is not unusual. 

Among the poor, and those who have become dependent because of 
the disease, we meet with a large number of patients who have no 
family to care for them during their illness and, with or without funds, 
they are unable to find lodgings under present conditions of rampant 
phthisiophobia. Many boarding houses bar persons who cough; and 
at times even near relatives are overtaken with a sense of stupid fear 
of infection, and want to get rid of the unfortunate patient. For these 
there is left nothing but to go to a well-regulated sanatorium. 

There is a large number of phthisical patients who notoriously lack 
will power to carry out the most important of the measures prescribed 
for them and, remaining in the city, they are apt to be tempted by 
the opportunities for gay life, or even excesses. They are better 
off in sanatoriums. 

On the other hand, there are many who show all willingness to do 
everything that is conducive to the cure of the disease, but they 


732 INSTITUTIONAL TREATMENT 


have not the funds to pay for capacious rooms in a desirable part of 
the city, for good nourishment and medical attendance. Tuberculosis 
is after all the most expensive of diseases, not only for the special 
and costly nourishment and residence which are required, but mainly 
for the long time the patient must remain idle, and the savings of years 
may be exhausted before he can resume work. While most of these 
can be, and are, well cared for in the clinics, the day and night camps, 
found in every large city at present, we meet with many who, for 
obvious reasons, are better off in sanatoriums, at least for short stays. 

Most phthisical patients should leave the city during the hot summer 
months, and those who cannot raise the funds for the purpose are 
proper charges of the sanatoriums. Indeed, if the sanatoriums were 
not filled with lazy, undeserving tramps and vagrants who remain for 
years in the institutions, and when discharged from one, soon gain 
admission to another, they could well care for the just mentioned class 
of patients. It seems to me that the German system of admitting 
tuberculous patients for three or four months is much superior to ours, 
where they are often kept indefinitely. The result is that the patients 
must wait for months before beds are vacant for them, and truly 
incipient cases, left without proper care while waiting for admission 
may become advanced. 

The longer we are up against the problems presented by tuberculosis 
in the city, the more we are convinced that the public sanatoriums 
ought to be converted into hospitals which admit patients on short notice, 
keep them for a few weeks, a month or two, until they regain their strength, 
and are fit for treatment in the clinics. Patients who suffer from acute 
exacerbations during the long, chronic course of phthisis could then 
be cared for. Inasmuch as municipal institutions are now in abundance 
near cities, this could easily be accomplished. 

But sanatoriums still work on the theory that they are to cure their 
patients, which they cannot do in more than 5 or 10 per cent of cases, 
which is, in fact, not more than home treatment accomplishes. 


CHAE eT Hero Le 
DIETETIC TREATMENT. 


Economic Aspects of Dietetics for Consumptives.— Because phthisis 
is accompanied by wasting of the body it requires careful, generous, 
and at times excessive nourishment with a view to covering the deficit 
created by the extravagant drain resulting from the toxemia, fever, 
loss of appetite, disturbed digestion, faulty metabolism and con- 
comitant emaciation. Cornet suggests that the rapid waste of the 
tissues tends to hasten absorption of the proteins surrounding the 
tuberculous foci and thus, at the same time, inhibits the natural pro- 
cess of healing by means of induration and also furthers the periph- 
eral dissemination of the bacilli. Inasmuch as the disease finds 
most of its victims among the poor and destitute, or causes destitution 
and despondency in those who had been self-supporting before its 
onset, the dietetic problems are not only of a physiological nature, 
but also have important economic bearings. It is self-evident that a 
dependent consumptive must not be prescribed food which is beyond 
his reach financially. 

In my experience the dietetics of phthisis is, in fact, more depen- 
dent on the financial resources of the patient than on the careful calcu- 
lation of the number of calories contained in the various foodstuffs. 
Considering the variety of dietaries which have been urged in this 
disease by various authors, and that each author claims good results 
with his method, it is obvious that no specific diet has been devised which 
will swt every case. In fact, all that can be stated is that tuberculous 
patients need food, just like other persons who are underfed, but they 
usually need more of tt. 

Need for Individualization of Diet.— Most of the studies in the 
dietetics of phthisis have been carried out in sanatoriums, some of 
which have had sufficient funds for an extravagant diet, while others 
with meager finances are alleged to have shown similar results. But the 
lessons from institutional experience are not applicable in their entirety 
to patients treated in their homes. On the other hand, the time- 
honored advice given to tuberculous patients: “Eat plenty of milk, eggs 
and meat,” is often decidedly harmful to those who follow it implicitly. 

There is great urgency for indindualization of the diet in phthisis; 
it is important that the diet should be adapted to the needs of the 
patient, and not to the disease. The “personal equation” counts for 
more than the disease. 

There is no doubt that the failure of institutional treatment of 


734 DIETETIC TREATMENT 


phthisis is, in a large measure, due to negligence in this regard. Whole- 
sale feeding is usually disastrous for human beings. The food in 
first class table d’héte restaurants is usually unbearable to the average 
healthy person, when relied on continually for a considerable time. It 
is impossible to make up a menu which will suit the palate, digestive 
capacities, and functions of one hundred patients in an institution 
where they must remain for months. The difficulties are greater with 
tuberculous patients whose gastric function and capacity for assimila- 
tion of ingested food are very often deranged. Tuberculous patients 
‘annot be treated like soldiers in the army, or prisoners, if we are to 
succeed in our aims. 

It is not true that two kinds of food of different composition, but 
theoretically of the same nutritive value, will invariably be of the 
same digestibility, or produce the same effects as regards nutrition. 
It may be calculated in the laboratory that a portion of beefsteak, 
roast beef, poultry, sausages, stew, cheese, potatoes, cereals, bread, 
milk, eggs, etc., contains a certain proportion of proteins, fat, and 
carbohydrates, and will liberate a certain number of calories when 
burned in the body. In fact, we know that the intrinsic value of three 
eggs is equivalent to about 100 grams of red meat, while 100 grams of 
bread is approximately equal to one egg, or 30 grams of beef, or 200 
grams of potatoes, or 280 grams of milk. But very often a consumptive 
assimilates three boiled eggs more easily than 100 grams of beef, or 
300 grams of bread. At times the patient assimilates 250 grams of 
milk better than 200 grams of potatoes. On the other hand if he has 
tuberculous ulcerations of the intestine he may not be able to digest 
and assimilate milk and eggs, but beef or poultry are digestible. 
Because of the personal equation many patients refuse to thrive on 
scientifically prepared dietaries. An Irishman resents spaghetti, an 
Italian refuses Irish stew, a German prefers sausages to the English 
roast beef, etc. 

For these reasons, in prescribing a diet for a patient we must always 
take into careful consideration his habits of life, the foods upon which 
he has been raised, and his personal likes and dislikes. Even when a 
change is imperative, it is dangerous to institute it suddenly, and 
we must make a strong effort to fit the diet to the one the patient 
has been used to. The factors which should guide us are the presence 
or absence of anorexia, fever, constipation, diarrhea, ete. 

Superalimentation and Forced Feeding.— With a view of replenish- 
ing the wasted tissues, especially in those who are by nature bad eaters, 
it has been suggested that superalimentation, or even forced feeding, 
is indicated in most cases of phthisis. It has been observed that 
occasionally an emaciated patient gains in weight under such a regimen, 
and some authors have advised that all sufferers from phthisis should 
be “stuffed.” Even Debove’s method of introducing food through 
the stomach tube into those who would otherwise not consume large 
quantities of nourishment was in vogue for some time until it was 


ESTIMATION OF THE NUTRITION OF THE PATIENT 735 


found that the gain in weight which forced feeding produced in some 
cases was not necessarily an indication that the lesion in the lung had 
improved. It was also found that many patients under forced feeding, 
with or without the stomach tube, may gain in weight and improve 
otherwise for some time, when suddenly the gastro-intestinal tract 
rebels, and within a few days they lose more than they had gained in 
several months. 

Estimation of the Nutrition of the Patient.—In our attempts at 
estimating the results of certain dietetic methods in tuberculosis we 
cannot always be guided by the scientific determination of the number 
of calories ingested by the patient every day; nor even by the quantity 
of proteins, fat, and carbohydrates which the patient has consumed. 
Attempts along these lines have proved futile in practice; they have not 
given us a diet which will suit all, or the vast majority, of cases. It 
seems that only clinical observation of the individual patient, his state 
of nutrition, his digestive capacity and the assimilability of the ingested 
food are of value in this regard. 

We aim at increasing the amount of nourishment so that the patient 
shall gain in weight and remain stationary at somewhat above his 
usual, or normal, weight before the onset of the disease. While in 
the vast majority of cases a gain in weight is a good index of the 
value of the diet, it is, however, often liable to mislead. Fattening by 
no means goes hand in hand with enhancing the resistance against the 
tuberculous toxemia in every case. We meet with cases with hardly 
any gain in weight, in fact remaining under the standard weight, yet 
the lesion in the lung heals, and recovery is good. 

“The main object of dietetic treatment,” says Brown,! “is to enable 
the patient to regain his lost weight, but not to make him a flabby, 
breathless mass of inert fat.” Excessive nourishment, which increases 
the weight of a patient more than two or three pounds per month 
on the average, is apt to result in an overload of fat and water without 
any utility. We should strengthen, but not fatten the patient. 
“When a workman has to perform hard work, he eats meat,” says 
Daremberg;? “the consumptive has to perform a very hard task, the 
task of repairing his wasted body.” In fibroid phthisis obesity is not 
rare—‘ obésité toxique”’ of the French—and is often more annoying to 
the patient than the symptoms in the respiratory organs. 

In the average case we may judge the progress of the disease by 
following the weight of the patient, provided we also take other factors 
into consideration. With the increase in weight there should also be 
an increase in strength; physical examination should show regression 
of the signs in the lungs, the cough should be ameliorated, and the 
quantity of sputum decreased. With such signs, a slow and persistent 
gain, finally reaching ten to fifteen pounds higher than the patient’s 





Osler’s Modern Medicine, 1, 482. 
Les differentes formes cliniques de la tuberculose pulmonaire, Paris, 1905, p. 149. 


1 
2 


736 DIETETIC TREATMENT 


normal weight before he was attacked by phthisis, indicates that we 
may be satisfied that the diet is good. 

Do All Tuberculous Patients Need Special Diets ?—A large propor- 
tion of phthisical patients, probably one-third of all, have good appe- 
tites and digestion. In fact, even febrile consumptives are seen without 
anorexia which accompanies nearly all other fevers. The prognosis 
is good so long as they retain their normal gastro-intestinal functions. 
They may be told that a moderate increase in the quantity of food they 
have been accustomed to eat is sufficient and, when possible, they 
should increase somewhat the quantity of proteins and fats, provided 
the stomach does not rebel. 

If the constitutional symptoms are in abeyance, or disappearing, 
and the signs in the lung show that the lesion is cicatrizing, we should 
not worry about a lack of gain in weight, or even when they remain 
a few pounds less than their normal weight. A patient with a good 
appetite and digestion needs no special diet; he should eat just like 
any other person, or a little more, if he can without inconvenience. 
On this point all authorities agree today. Thus, King' says: “In the 
absence of certain complications, a diet which would suffice for the 
same individual under normal conditions of life will doubtless, with 
very slight modifications, meet the requirements in the presence of 
tuberculosis, the more especially during that period of the disease 
when constitutional symptoms are either absent, or but slightly mani- 
fest.” Paterson,? whose patients work at graduated labor, gives 
them “a liberal diet which consists of the ordinary food which the 
working classes provide for themselves when they are in a position to 
afford it.’ In fact, patients who tend to become excessively fat have 
their diet reduced in quantity. 

On the other hand, patients who lose progressively in weight and 
strength, are anemic and debilitated, despite the rest which is rigidly 
enforced, need more and better food if they are to recover, or hold their 
own, in the struggle with the disease. But even here superalimenta- 
tion must be carefully adapted to the digestive capacity of the patient. 

It may be stated, as a general rule, that the suggestion of some 
authors that in such cases the patients must consume between 4500 
and 6000 calories daily is a dangerous one. Experience has taught 
that one who will not recover, or hold his own, on a diet of 3500 calories, 
will not recover at all. N. D. Bardswell and John E. Chapman? 
have arrived at the conclusion after a thorough experimental study of 
the subject that 3000 calories per day are quite sufficient. 

Variety.—The first principle to be observed in the diet of the tuber- 
culous patient who is losing weight is variety, both as regards nutritive 
principles as well as appetizing qualities. There is nothing more 
abhorrent to a tuberculous patient, and to a large extent to all sufferers 


1 Sixth Internal. Cong. Tuberc., 1908, 1, 719. 
2 Tbid., p. 893. 
3 Diets in Tuberculosis, London, 1908. 


PRECAUTIONS TO BE TAKEN IN OVERFEEDING PATIENTS 737 


from chronic diseases, than homogeneity of diet. No limited and 
exclusive diet can keep a patient well for any length of time because 
it does not respond to the urgent demands of the different organs and 
tissues of the body. It does not stimulate the secretions of all the 
digestive glands. If an exclusively animal diet is taken, only the 
gastric Juice is stimulated, while the saliva, pancreatic juice, bile, and 
intestinal juices are not utilized and, remaining free in the gastro- 
intestinal tract, are apt to act as irritants and produce diarrhea which 
is exhausting, or constipation which is harmful in other ways. 

We often meet with patients who have been given diet lists in 
which four or five meals are listed for the day. But any appetite 
they may have had before the list was consulted promptly disappears, 
because it shows the foods which have been given them for months 
without any appreciable variation. Many patients who have followed 
the injunction “plenty of milk and eggs’ have engendered such an 
aversion to these articles that the mere mention of an egg is sufficient 
to disturb the slight appetite for other foods which was called forth 
by hunger. It is always advisable to consult the patient as to the kind 
of food he prefers or longs for and, if there are no contraindications, 
to give it to him. 

Precautions to be Taken when Overfeeding Patients.— Before a 
patient is urged on to a course of superalimentation certain precau- 
tions are to be taken: He must be carefully examined with a view of 
ascertaining whether or not he can stand additional feeding. Those 
showing signs of arteriosclerosis, nephritis, gall-stones, nephrolithiasis, 
or gout, should not be allowed superfeeding, especially with animal 
proteins. It is likely to throw a considerable strain on the kidneys, 
or even produce albuminuria. Moreover, as we have seen, patients 
with these diseases do rather well when affected with tuberculosis 
(see p. 602). The condition of the stomach is to be ascertained, and 
those having dilated organs, or disturbances in the tonicity and motility 
of the viscus, are to be treated for these troubles when practicable. 
The appetite is of great importance. Although we may succeed with 
some patients in urging them to eat irrespective of the appetite, we will 
fail with many. 

Proper preparation of food goes a long way in counteracting anorexia; 
Dettweiler, who made a great success with his sanatorium, said that 
the kitchen was his pharmacy. It is to be regretted that very few, if 
any, modern public sanatoriums are conducted on this principle. 
It is better to give the patient small quantities of each of several dishes, 
well, and appetizingly prepared, than large quantities of one or two 
dishes. The fact that the food value is theoretically sufficient in the 
latter case does not alter matters. With some patients animal food 
should predominate, with others eggs, and with still others, milk. The 
diet must be frequently changed, especially when the digestive tract 
shows signs of rebellion. 

With well-to-do patients these are simple matters, but with those 

47 


738 DIETETIC TREATMENT 


of limited means this problem is often hard to solve. The writer 
usually sends for the mother, wife, or sister of the patient and gives 
her directions along these lines. 

Bearing in mind that the disease is likely to last for months, if not 
for years, we must spare the digestive organs, the cornerstone of 
phthisiotherapy, as they have been called, and not overburden them 
with work. The first imperative principle is proper mastication. 
But regularity in meals is of the same importance. The menus of 
some authors mention six and more meals a day, which are excessive, 
in my experience. Three, at most four, meals a day are sufficient for 
most patients, and afford some rest to the stomach between the meals. 
At all events, the stomach must be given a complete rest during the 
night, which can be done by avoiding all food between 9 P.M. and 7 A.M. 

Protein Foods.— Experimental researches of Richet and Hericourt, 
and others, have proved conclusively that when ingested raw, animal 
foods have an especially beneficial effect in tuberculosis. The specific 
effect seems to reside more in the juices of the meats than in the fiber. 
Herbivorous animals, like the cow, are more prone to tuberculosis 
than carnivorous animals, as the dog. 

The best source of proteins for a tuberculous patient is animal 
food; the proteins of vegetable origin are not so easily assimilated. 
Meats possess all the qualities which are necessary for the nutrition 
of the consumptive. To be sure, there are some who maintain with 
Kellogg! that a low protein diet is productive of better results, and urge 
vegetable proteins in the dietetic management of the malady. It is, 
however, an every-day observation that the animal proteins do not 
tax the digestive organs to excess and, excepting in those who suffer 
from some form of dyspepsia, they can be taken by most consumptives 
without difficulty in comparatively large quantities. Beef, mutton, 
lamb, poultry, game, fish, oysters, eggs, milk, cheese, etc., offer a wide 
range of choice for variety. 

Those who have no natural abhorrence for raw meat may have it 
with great benefit—zomotherapy was at one time very popular, espe- 
cially in France, and may be utilized, when tolerated. Some patients 
are not averse to taking a small piece of raw beef, dipping it in tomato 
sauce, and eating it. It is, however, better to mince or chop it, and 
eat it between two slices of bread as a sandwich, but it should be sea- 
soned to taste. The vast majority of patients, however, prefer roasted 
or boiled beef, mutton, poultry, ete. It must be mentioned that when 
roasted or broiled, meats should be rather underdone and, on the whole, 
they should be changed often in kind and in the form prepared for the 
table. 

But it should never be excessive; we cannot rely on animal foods 
exclusively in nourishing a tuberculous patient. To supply a patient 
with 5000 calories per day, it would be necessary to gorge him with 


1 Sixth Internat. Cong. Tuberc., 1908, 3, 740. 


PROTEIN FOODS 739 


six and a half pounds of meat, or thirty-six eggs, or five quarts of 
milk, or two pounds of cheese. This would be too much—no human 
being could take it with impunity for any length of time. For this 
reason other foodstuffs are necessary in addition to the animal food. 
The most the average consumptive should have is about three-fourths 
to one pound of animal food, and when meat is taken raw, it should 
not exceed one-half pound per day. When this is taken with one pound 
of bread, three eggs, one quart of milk, eight ounces of potatoes, and 
four ounces of fresh vegetables, and some fruit, the diet is complete. 

Attempting to feed tuberculous patients with proteins we are often 
confronted with the high cost of animal foods. In many cases we may 
attempt to supply proteins from fish, which are much cheaper than 
beef, veal, or poultry. Now, beef contains from two to three ounces 
of protein per pound. Fresh fish, such as haddock, cod, halibut, perch, 
salmon, mackerel, or shad, contain from one-and-a-half to two-and- 
a-half ounces, while the commoner dried fish contain even more pro- 
teins, up to three ounces per pound. Proteins in a digestible form 
may thus be purchased, when fish are used, at from 30 to 50 per cent 
of the cost of the same amount when consumed in meats. In fact, 
Drummond! has shown that the coagulable proteins of the muscle 
tissue of cod, herring, and canned salmon have a nutritive value as 
high as those derived from beef. The empiric experience of the 
therapeutic value of cod-liver oil in tuberculosis has also recently been 
reinforced by the investigations of Osborne and Mendel? who dis- 
covered in fish one of the important vitamins, the fat-soluble A, which 
has such an immense influence on the growth and health of the animal 
body. Drummond urges, therefore, the so-called “fatty” fish, which 
contain considerable quantities of fat distributed throughout their 
muscle tissue, as important foods containing the fat-soluble vitamin. 
The herring is especially to be recommended from this angle. Either 
for the sake of variety, or because of imperative saving in cost, fish 
should not be neglected from the diet of the tuberculous. 

A consumptive needs more protein foods than a healthy person 
because the disease destroys the tissues, especially the muscles, and 
there are no better tissue builders than proteins. But we must not give 
them at the expense of other foods. It is unnecessary, even dangerous, 
to give more proteins than are required for repairing the tissues; other- 
wise they are likely to prove more disastrous than to a healthy individual. 
These evils are, as the researches of Chittenden, Mendel, Folin, Herter, 
Metchnikoff, Tissier, Combe, Turk, and others show: (1) That 
protein which is not used for tissue building is not “burned clean,” 
as are fat and carbohydrates, which yield merely water and carbon 
dioxide, but leaves behind “clinkers”’ in solid form—for instance, uric 
acid; (2) that meat proteins also contain such ‘“clinkers” in their 
extractives, which are superadded to the similar products from the 


1 Jour. of Physiology, 1918, 52, 95. 
2 Jour. Biol. Chemistry, 1914, 17, 401, 


740 DIETETIC TREATMENT 


metabolism of proteins in the body; (3) that all protein which is not 
absorbed is subject to putrefaction in the intestinal canal, and gives 
rise to toxins which are partially absorbed and produce injuries of 
various kinds to the organism (Irving Fisher). 

Milk.—Milk has been considered for centuries a good food for 
consumptives—Aretaeus, eighteen hundred years ago already spoke 
of it favorably in this connection. It contains more than 10 per cent 
of nutritive matter, albumin, fat, sugar, and salts. But this does 
not mean that it is good to use it exclusively for our patients as has been 
done in the well-known “milk cures.” If we wanted to supply all the 
requirements of a patient it would be necessary to make him ingest 
five to seven quarts of milk per day. In a few weeks his stomach 
would be dilated two or three times its normal dimensions. 

But with other foodstuffs it is excellent because its nutritive prin- 
ciples are easily digestible in the stomach and intestines, and it contains 
no toxic substances. It is just as good for a patient with fever as 
for one who is afebrile. A quart of milk is equivalent in fuel value 
to a pound of lean meat, or eight eggs. It is thus evident that, from a 
certain standpoint, it is a much cheaper source of fuel than either 
meat or eggs. 

It is best given between meals in the form of drink, and may be 
added to many other foods, especially cereals. But it must not be 
abused; patients who gorge themselves excessively with milk lose 
their appetite for other foods. Between a pint and a quart of milk 
per day is to be considered the maximum for the average patient. 

There are patients who do not bear milk very well. In some it pro- 
vokes lactic and butyric acid fermentation in the stomach; this viscus 
becomes dilated, and the complicating hyperchlorhydria favors 
spasmodic contraction of the pylorus. In others, the milk clots 
excessively in the stomach, large solid curds are formed which irritate 
the mucous membrane and cause nausea and vomiting. In some 
patients the milk passes the stomach without difficulty, but it pro- 
duces trouble in the intestines—gaseous distention and diarrhea. I 
have seen many cases of diarrhea in consumptives, which were thought 
to have been caused by intestinal ulcerations, but which disappeared 
with the withdrawal of milk from the diet. 

The milk may be rendered more digestible by diluting it with alka- 
line waters, or lime water, but then the total quantity consumed must 
be reduced. It is usually more easily digested when given with some 
cereal, like oatmeal, or rice. Atwater found that milk is more easily 
digested when it is part of a mixed diet. When consumed alone the 
proportion digested was: proteins, 91.2 per cent; carbohydrates, 
86.3 per cent; and fat, 92.8 per cent. When milk and bread made 
up the diet, the amount digested was: proteins, 97.1 per cent; carbo- 
hydrates, 98.7 per cent; and fat, 95 per cent. 

Fermented milk is often more easily borne in large quantities when 
the pure article is not sustained, We may try koumiss, keffir, or the 


EGGS 741 


various preparations of buttermilk, which are at present supplied by 
most milk dealers at reasonable prices, or may be prepared at home 
with cultures or tablets of lactic acid bacilli. 

Cheese is an excellent food for consumptives. But we should avoid 
the highly seasoned varieties. Cream cheese and ordinary pot cheese 
contain considerable nutritive elements and do not provoke cough or 
gastric irritation. 

Eggs. — Eggs are considered an excellent food for tuberculous patients 
by the profession and the laity. In assimilability they exceed any 
known food excepting milk and oysters. They contain enormous 
quantities of albumin and fat. The white of an egg consists of pure 
protein which is as digestible and nourishing as that of beef; the yolk 
contains 25 per cent of fat, 15 per cent of protein, and also nuclein, 
lecithin, iron, and salts. Eating one dozen eggs per day, a consump- 
tive could feed himself, and pushing it to twenty eggs he would absorb 
the equivalent of two and a half pounds of beef, because an egg of 
50 grams is equivalent to about 35 grams of moderately fat beef, or 
128 grams of cow’s milk. In other words, they contain over 700 
calories per pound; the whites yield 250 and the yolks 1700 calories 
per pound. But an exclusive egg diet is just as bad as an exclusive 
meat diet. Too much fat is introduced into the stomach and con- 
gestion of the liver is the result, while with an exclusive meat diet, 
congestion of the kidneys occurs. 

It appears, however, that eggs have been abused as an article of 
food for the tuberculous. Many of the gastric derangements of 
tuberculous patients can be traced to the abuse of eggs as a food. 
Most patients consume them raw, and it has been found that raw 
white of egg is decidedly indigestible. Mendel and Lewis! pointed out 
that, when given to animals, raw eggs give rise to diarrhea. W. G. 
Bateman? found that in dogs, when given in considerable quantities, 
it sometimes causes vomiting and invariably produces diarrhea. 
Pawlow found that raw white of egg only partly stimulates a flow of 
gastric juice. But Bateman shows that cooked egg-white, on the con- 
trary, calls forth an abundance of juice and unites easily with hydro- 
chloric acid. Egg-white remains but a while in the stomach, and 
escapes in gushes through the pylorus. “Once in the intestines the 
native egg-white continues to oppose the digestive enzymes, for it has 
remarkably strong antitryptic properties. . . . Not only does it 
resist digestion itself, but it prevents the digestion of other easily 
digested proteins.” It is very poorly utilized. In large doses, from 30 
to 50 per cent of that ingested is wasted by being ejected with the 
feces. In normal feces albumin is never found. In contrast with egg- 
white, egg-yolk has been found to be well digested and utilized. 

Clinicians who have the care of tuberculous patients should there- 
fore heed the following warning of Bateman: ‘A substance which 


1 Jour. Biol. Chem., 1913, 16, 55. 
2 Tbid., 1916, 26, 263; Am. Jour. Med. Sci., 1917, 153, 841. 


742 DIETETIC TREATMENT 


fails to stimulate a flow of gastric juice and is antipeptic, which hurries 
from the stomach, calls forth no flow of bile, and strongly resists the 
action of trypsin, which is poorly utilized and may cause diarrhea, has 
evidently little to recommend it as a foodstuff of preference for the 
sound person, let alone for the invalid.” 

On the other hand, cooked egg-white is easily digested and well 
utilized by the economy. All that is necessary to prepare egg-white 
for digestion is to heat it to 70° C. Under no circumstances should a 
tuberculous patient be permitted to consume several raw eggs a day. 
They should invariably be boiled. In fact, in my experience eggs may 
be fried, scrambled, or prepared in any way; so long as they are not 
consumed raw, they make an excellent food for tuberculous patients. 

But there are some exceptions. Those who suffer from derange- 
ment of the function of the stomach and the liver do not bear eggs very 
well and they may have to be discarded. ‘The same is true of patients 
who have an idiosyncrasy to eggs and get colicky pains in the abdomen, 
vomiting or diarrhea from an egg. 

Four to six eggs per day is about the maximum which a patient 
should be allowed, if we are to retain the functions of the stomach 
and liver. In most cases less should be given. 

Fats.— While the amount of fat necessary for the average consump- 
tive has been exaggerated by many authors, it is nevertheless a fact 
that a diet containing a surplus of easily assimilated fat is the best. 
It must, however, be borne in mind that the capacity for digesting 
and assimilating fat varies with the individual. In some patients 
an increase in the amount of fat is immediately followed by gastro- 
intestinal disturbances. Many people cannot digest fat meats like 
bacon, ham, etc. We have already mentioned that many patients 
have shown intolerance for fat even before the onset of the disease. 

I have found that butter is superior for our purposes, and it has given 
me results as good as cod-liver oil, which has been popular for centuries. 
I direct my patients to cut their bread in thin slices and cover them 
with heavy layers of butter; mixing butter with mashed potatoes and 
other foods. As much as six to eight ounces of butter can thus be 
consumed daily by the average patient without gastric or intestinal 
disturbances. Those who like to and can consume large quantities of 
unskimmed milk may get the greater part of their fat in this manner, 
while cream and certain kinds of cheese are also rich in fat. In look- 
ing for sources of easily digestible fat we must not forget fish: salmon, 
pompano, sardines, shad, fish roe, caviar, etc., are very good for this 
purpose. Those who have great tolerance for fat may also take in 
addition to butter, cream, cream cheese, fat meat, and bacon. 

The quantity of fat a patient should consume varies according to 
the season, the kind of food he has been accustomed to eat, h s tolerance 
of fat, and the condition of his gastro-intestinal tract. Of course, 
those who are obese, and they are not rare among those with quiescent 
and healed lesions, should be discouraged from eating an excessively 
fat diet. 


SALTS 743 


It has been my experience that a patient without preéxisting gastric 
disease can consume six ounces of fat every day for months with bene- 
fit. But now and then one is met who shows a decided inclination to 
fat intolerance. It is my impression that in most cases it is due to the 
excessive amounts of improper fats which have been forced upon 
them. It has been suggested by Tibbles that when a patient cannot 
take fat, the proteins can be increased; 100 grams of proteins will 
yield 40 grams of fat. on alone will never fatten a patient; 
6.5 pounds of lean meat, or 5.5 pounds of lean and fat meat would be 
required to supply the daily requirements of carbon for an ordinary 
person; therefore some other source for fat must be found. 

We must guard against quick fattening, “stuffing,” of tuberculous 
patients. Often consumptives are urged to eat plenty and some ingest 
enormous quantities of food and gain remarkably well. Taking their 
weight weekly, and finding that it keeps on increasing, they are 
encouraged to continue in this manner, and at the end of three or four 
months the gain may be as much as thirty or even forty pounds. But 
to their dismay they have not been rehabilitated in other respects; 
they are as yet unable to work, and are, in fact, weaker than before. 
The weight they have put on is only an added burden, which is not 
only useless, but actually incapacitating. In addition, they suffer from 
annoying dyspnea. Physical examination shows that the process in the 
lungs has not improved; perhaps it has distinctly extended. Carefully 
and guardedly reducing these patients has often been of great benefit. 

Carbohydrates. —In the eagerness to supply the body of the patient 
with proteins and fat, carbohy drates must not be neglected from the 
diet. They are, as a rule, easily digested and eeintilereds and they 
spare the proteins, thus maintaining the nitrogen balance, or equilib- 
rium, with smaller quantities of proteins. The best sources of 
carbohydrates are potatoes, cereals—like oatmeal, rice, etc., which 
may be taken with milk or cream—pastries, and above all, bread. 
Cane sugar and maple sugar, which enter into various culinary prepara- 
tions, are of great value. Daremberg,! however, objects to excessive 
consumption of sweets by consumptives because they are usually 
dyspeptics who do not stand it very well. He says that those who 
can take an excessive quantity of sugar may become fat rapidly; 
but this fattening is not lasting, just as the fattening obtained from 
an excessive milk diet. The best fattening is obtained from a mixed 
diet. However, there is no reason against eating sweet desserts, or 
even candies, in moderate quantities, provided they are taken after 
meals when they are not likely to interfere with the appetite. 

Salts.— Mineral salts must not be neglected. Even if the theory of 
demineralization is not well founded, there is no question that the 
loss of mineral salts is higher in consumptives than in healthy indi- 
viduals. Iron, lime, soda, magnesia, and the phosphates, are best 


1 Les differentes formes cliniques de la tuberculose pulmonaire, Paris, 1905, p. 157. 


744 DIETETIC TREATMENT 


supplied by such foods as bread, flour, oatmeal, rice, sago, tapioca, 
fresh vegetables, and fruits. All these may be given plain, or, better 
still, in various other culinary preparations. 

Condiments.—T’or their local appetizing effects, condiments, acting 
as they do as great salivary and gastric stimulants, may be taken, 
especially by those who suffer from anorexia. Some condiments, like 
mustard and garlic, contain allyl which assists in the digestion of fats, 
and is said to be bactericidal in the intestinal tract. At one time 
garlic was considered a good remedy against tuberculosis. Its active 
principle, allyl, was even administered subcutaneously. 

Dangers of Overfeeding.— While the majority of patients stand a 
moderate increase in the quantity of food fairly well, there are many 
who are decidedly harmed by it. This is especially seen in those who 
have been unreasonably induced to increase the quantity of protein 
foods, such as eggs, meat, etc., thus imposing an excessive, and often 
dangerous, burden upon the liver, kidneys, ete. In some cases we find 
that these organs have been decidedly crippled by such a diet. 

The symptoms produced by excessive protein consumption are 
unmistakable: The patient is drowsy for an hour or two after meals, 
has headache, and is irritable. At night he is restless and sleepless, 
or his sleep is disturbed by frightful dreams. The abdomen is dis- 
tended, the liver enlarged,and may be tenderonpalpation. Heartburn, 
anorexia, bilious vomiting, and diarrhea often torture the patient. 
Cardiac palpitation and nightsweats are, at times, due to the indiges- 
tion thus induced. Because of the plethoric condition, these patients 
often have epistaxis, and also hemorrhoids, which contribute to their 
misery. The urine contains albumin, biliary pigments, indican, and 
glycosuria is not rare. Arthralgic pains in the joints are often the 
result of superalimentation. Older clinicians, observing that there 
exists an antagonism between the gouty and phthisical diatheses, 
urged excessive nitrogenous diet combined with wines, with a view of 
inducing sclerotic changes in the diseased lungs. Ona similar principle, 
the excessive consumption of alcohol was advised in former days. 
According to some authors, the acneiform eruptions on the skin of some 
tuberculous patients are very frequently due to the excessive protein 
foods which they consume. 

When overfeeding a patient we must watch out for the following 
danger signals: Failure of appetite, and symptoms of flatulent dys- 
pepsia; dyspnea on exertion, which is obviously not due to the tuber- 
culous toxemia or the lung lesion; diarrhea, and at times vomiting. 
If these symptoms are not heeded, and forced feeding is continued, 
irreparable damage may be done; the sheet-anchor of the patient, 
his power to digest food, is damaged, and his chances of recovery are 
materially lessened. But this should not deter us from trying to feed 
the tuberculous patient generously. ‘Excessive feeding is clearly a 
vastly better method of treatment than underfeeding, for it at least 
ensures the consumptive taking enough to repair his waste and to 


DIETARIES 745 


restore his normal power of resistance and recuperation,” say Bards- 
well and Chapman,! “ The point to realize is, that it is quite an unneces- 
sary hardship for patients to be overfed, and that it may do positive 
harm.” 

When these harmful results of unwise feeding are borne in mind, 
unfortunate patients will not be forced to ingest large quantities of 
food which may be excessive and dangerous to healthy persons. Espe- 
cially careful must we be with plethoric, obese, and sedentary con- 
sumptives. A dilated stomach which does not empty itself with ease 
and promptness is particularly to be spared. The dangers of excessive 
ingestion of fat have already been dwelt upon. 

Dietaries.—I*rom what has been said, it is obvious that it is not 
necessary to give detailed dietaries for consumptives. When we aim 
at variety as the first requirement for a good diet, it would be neces- 
sary to give at least thirty menus to suit the average case. We will, 
therefore, merely mention some of the foods which may be utilized in 
attempts at feeding phthisical patients properly. It will be noted 
that they may eat nearly everything a healthy person can, so long as 
their malady is not complicated by conditions which alter matters. 

Breakfast.— Milk, coffee, chocolate, cocoa, or tea. Bread, butter, 
cream, eggs, bacon, ham, ox tongue, fish (fresh or canned), fruit of 
any kind. Plenty of butter. Cereals of any kind. 

Lunch.— Fish, or entrée; meats (roasts, chops, steaks, etc.), poultry, 
vegetables, custards, puddings, cheese, milk, coffee, fruit. 

Dinner.—Soups, meats, poultry, game, fish, all vegetables, puddings, 
pastries, ete., cheese, ice-cream, coffee, milk or chocolate. 

Without going into details of the various dishes that may be prepared 
by a good cook who knows the like and dislikes of the patient, it can 
be stated that there is no dish which is contraindicated in uncom- 
plicated phthisis. A good cook can do more for the patient than all 
the dietaries which may be printed in a book. 

Between the three main meals there may be allowed a light luncheon 
consisting of a glass of milk and some biscuit. Some are allowed an 
egg or two at that time, made in some form of punch, or in any style, 
provided it is well borne. Similarly, at about 4 p.M., tea, coffee, or 
milk may be allowed with some biscuit, etc. At night before retiring, 
a cup of milk with some crackers is beneficial for some patients. It 
will be noted that in this manner the patient may have his milk— 
about one-half to one quart per day—mainly outside of his meal-time, 
as drinks. 

It must be emphasized again that these foods should be palatably 
prepared and rendered digestible by proper cooking. Otherwise 
trouble may arise. The quantity to be ingested depends on the per- 
sonal equation of the patient, although in some cases matters may 
be forced for some time when indicated, but this should only be done 
bearing in mind the contraindications which have already been 
discussed. 

1 Diets in Tuberculosis, London, 1908, p. 49. 


CG TH AcP a iy excise 
MEDICINAL TREATMENT. 


Importance of Medicinal Treatment.—The disrepute of medicinal 
substances in phthisis during recent years is due to several causes. The 
first and most important is that we have no specific botanical, chem- 
ical, or physical agent which, when administered to a consumptive, 
will exert a selective action on the tubercle bacilli, as mercury and 
arsphenamine do on the spirocheta of syphilis, and quinine on the mala- 
rial parasite. Nor have we a therapeutic agent which will enhance 
the resistance of the tissues against the ravages of the tubercle bacilli, 
or neutralize their poisons, or stimulate sclerosis of the affected area. 
But here we are in about the same position as when dealing with 
anemia, typhoid, pneumonia, rheumatism, etc. When we find that the 
salicylates relieve the most painful symptoms of rheumatism, and 
that iron increases the hemoglobin content of the erythrocytes in chlo- 
rosis, that digitalis increases the force of the cardiac muscle, we use 
these drugs although we know that digitalis does not regenerate 
destroyed heart valves, and salicylates do not remove the essential 
cause of acute articular rheumatism. Similarly if we find that creosote, 
arsenic, ichthyol, etc., have a beneficial influence on some of the annoy- 
ing clinical phenomena of phthisis, though they do not cure the disease, 
we must not discard them merely because they do not remove the 
cause of tuberculosis, or kill the bacilli within the body, or neutralize 
the tuberculous poisons, ete. 

There is another aspect to be considered in this connection. Except- 
ing the chosen few, who have sufficient means to pay for first-class 
sanatorium treatment, and inclination to remain in the institution for 
months and perhaps years, the bulk of the patients must be treated 
in their homes. Even if they get a few months of sanatorium treat- 
ment in a public institution, they must be treated in dispensaries, 
or by their family physicians, before admission, and after discharge. 
The patient is a human being; and when we consider the human 
element we find that, as a rule, he has no confidence in a physician 
who has no remedy for his ailment. The dictum “plenty of fresh 
air, milk, and eggs,’ he believes he knows as well as the physician. 
If his medical adviser will not prescribe for him, he will seek remedies 
from another who is more obliging in this respect, or from an advertis- 
ing quack. This is not only true of the ignorant, but also, almost to 
the same extent, of the supposedly intelligent patient. 

It cannot be denied that in many respects medicaments, properly 


CHEMOTHERAPY T47 


administered, act by psychic suggestion. But so do the minute and 
detailed directions given, often in writing, about diet, rest, exercise, 
sleep, etc., in institutions. ‘‘ Medicinal agents,” says G..Niiss,' one 
of the most ardent advocates of tuberculin treatment in France, 
“no matter in what they consist, always inspire confidence in the 
physician; without them he is helpless. Moreover, by giving the 
patient, in addition to other treatment, a prescription calling for some 
medicine, we may succeed better in our attempts at keeping him 
away from the alluring advertisements of charlatans who very often 
impose on him.” 

Harmless Medication.—The reasons why medicinal agents have 
fallen into disrepute in medical literature—by no means in the practice 
of the vast majority of physicians—are manifold. But the most 
important is perhaps the fact that drugs have been abused. “I regard 
medication as indispensable in the treatment of tuberculosis,” says 
Rénon. “It has an undoubted good effect on the disease in general 
and an enormous psychic effect. But there is one important condi- 
tion which must be realized above all when giving drugs to consump- 
tives—they must be harmless.” He illustrates this point by the fol- 
lowing instance: Some years ago the acetate of thallium was suggested 
as an excellent remedy against the nightsweats of phthisis, and a trial 
showed that it did control this symptom very well indeed. But it 
also had another effect: It caused the hair to fall out, and the nails 
to shed. The patients stopped sweating, but incidentally lost their 
hair and nails, which was a good reason for resentment. That certain 
drugs used in phthisiotherapy may have disastrous effects in addition 
to their influence on the disease, or some of its symptoms, must always 
be borne in mind. In fact, it has been stated with considerable truth 
that 50 per cent of the dyspepsia in phthisical patients is due to 
improper medication. 

Chemotherapy.— Ever since the bacterial origin of tuberculosis has 
been proved by Koch, attempts have been made to find a pharmacologi- 
cal agent which will destroy tubercle bacilli within the infected organism 
without simultaneously harming the host. Of course, the well-known 
antiseptics and bactericides inhibit the growth of the bacilli in vitro, 
and kill them in even great dilutions. But, for obvious reasons, the 
administration of these substances to animals or humans for thera- 
peutic purposes is unthinkable. Indeed, it has been found that all 
substances known to inhibit the growth of tubercle bacilli in cultures 
fail to prove of therapeutic value in experimental tuberculosis in 
animals, and in spontaneous disease in human beings. 

During recent years, since the great achievements of Ehrlich in the 
chemotherapy of diseases caused by protozoa, renewed attempts 
have been made to find a synthetic substance possessing a selective 
affinity for the cytoplasm of the tubercle bacillus without simulta- 


1 Gilbert and Carnot’s Therapeutique, 21, 594. 
2 Le traitement pratique de la tuberculose, Paris, 1908, p. 110. 


748 MEDICINAL TREATMENT 


neously harming the cells of the patient. But great stumbling blocks 
have been encountered in these attempts. To begin with the tubercle 
bacillus is surrounded by a fatty capsule, making it impermeable to 
the action of mild bactericides. Attempts at using lipolytic agents 
for the purpose of dissolving the waxy envelope of the tubercle bacillus 
have, so far, not met with encouraging results, especially in living 
organisms. Another hindrance to successful chemotherapy in tuber- 
culosis is the fact that the tubercle is an avascular structure, as was 
shown when discussing the morbid anatomy of the disease. To reach 
the tuberculous lesions the remedy must be carried by the blood or 
lymph stream, irrespective of the route by which it is introduced into 
the body. 

On the other hand, some authors have argued that avascularity 
may be altogether useful in chemotherapy by favoring the accumula- 
tion of the drug in tuberculous tissues. That this is feasible is seen 
in the fact that certain substances, as calcium salts, do enter tubercles 
and remain there. They are part of the natural mode of healing tuber- 
culosis, and a therapeutic agent may likewise be brought into the 
diseased tissue. But, so far, no substance has been discovered which 
will penetrate the tuberculous tissues and remain there for a sufficiently 
long time to exercise beneficial effects. 

It has been found by many authors, notably Wells and Hedenburg,! 
that the permeability of tuberculous tissue is like that of any simple 
colloid, permitting crystalloids to diffuse readily through them, but 
that it is hardly permeable to colloidal molecules. It has also been 
observed that tuberculous lymph glands take up relatively more iodine 
from the blood than other organs. Considering that iodine has been 
used for generations in phthisiotherapy, this was considered a hint in 
the direction of finding some synthetic compound of iodine which may 
prove of the same value in tuberculosis as arsenic, which also was used 
before the days of chemotherapy, in syphilis. But it was soon dis- 
covered that the deposition of iodine in tuberculous tissue is not entirely 
due to its selective affinity for the protoplasm of the tubercle bacillus, 
or the cells of tuberculous lesions, but that necrotic tissues caused by 
any other bacterial agent have the same proclivities, and that the 
amount of iodine found in necrotic tissue, tuberculous and others, 
depends mainly on a purely physical condition, the destruction of the 
semipermeability of the living cells. 

An enormous amount of work has been done with a view of obviating 
these hindrances to attacking the tubercle bacilli in the infected 
organism, but so far no results worthy of the efforts has been attained. 
All attempts at destroying the fatty capsule of the tubercle bacillus 
through the agency of lypolitic substances have failed to show thera- 
peutic results. The works of many indefatigable workers in Europe 


1 Jour. Infect. Dis., 1913, 11, 349. 


CREOSOTE 749 


and in this country, among the latter may be mentioned Lewis,! Wells,’ 
DeWitt,? and many others, using various elements, as copper, gold, 
iodine, etc., and various dyes, have so far not brought out a remedy 
which will cure or ameliorate experimental tuberculosis in animals, 
or spontaneous disease in man. Apparently the reason for this failure 
of chemotherapy is to be sought in the complex etiology of the disease. 
To be sure there is no tuberculous disease without tubercle bacilli, but 
as we have already shown (see Chapters IV and V), infection is followed 
by disease only in a comparatively small proportion of persons into 
whose bodies these bacilli have gained an entrance. It seems that a 
specific remedy will have to be directed against certain constitutional 
defects which render the body vulnerable and which we do not under- 
stand clearly at present, and not alone against the tubercle bacillus. 
But even here we are not on sure ground at the present state of our 
knowledge of phthisiogenesis. 

One thing must be emphasized in this connection. Many who have 
some drug which they believe effective in relieving some of the symp- 
toms of tuberculous disease do not hesitate to call it chemotherapy. 
In a certain sense this may be considered correct. But, as defined by 
those who work along these lines, chemotherapy consists in the intro- 
duction into the body of bacteriotropic substances which are not in the 
same degree organotropic; substances which though very harmful to the 
virus of the disease are hardly harmful, if at all, to the cells of the host. 
Such a substance is, at present, an ideal, a hope of many indefatigable 
workers. 

However, though no specific remedy has as yet been found for 
tuberculosis, there are many which are of immense utility in our 
efforts at relieving the symptoms which torture the patient. Some of 
these will be discussed here. 

Creosote.—There are but few sufferers from tuberculosis who have 
not been given creosote at some period of their illness. Its history is 
similar to that of tuberculin. Introduced by Reichenbach, in 1830, 
it was given in very large doses, resulting in considerable harm to the 
patients. It was discarded for this reason, to be reintroduced some 
thirty years ago, and ever since it has held its place in the armamen- 
tarium of the physician in general and special practice. Its most 
ardent advocates do not consider it a specific, but then those urging 
tuberculin are still looking for a specific for tuberculosis. In the hands 
of those who have administered it intelligently it has proved the best 
medicinal agent to relieve some of the most baneful symptoms of the 
disease. 

Those favoring this drug claim that when administered in the proper 
cases, and in proper dosage, it improves the appetite, stimulates diges- 
tion and assimilation, improves nutrition, diminishes expectoration, 

1 Johns Hopkins Hosp. Bull., 1917, 28, 120. 


2 Jour. Infect. Dis., 1913, 11, 349. 
3 Ibid., 1913, 12, 68; 13, 378; 22, 426. 


750 MEDICINAL TREATMENT 


removing, at times, its purulent character and disagreeable taste and 
odor, all of which are sufficient encouragement to the average sufferer 
from phthisis to bestow confidence in the physician, and to look forward 
to an ultimate recovery. Some earlier writers were inclined to ascribe 
this beneficial action of creosote to its power to inhibit the growth of, 
or destroy, tubercle bacilli in the gastro-intestinal tract, which are 
inev itably swallowed by every consumptive. For obvious reasons this 
isabsurd. But it isa fact that it is one of the best gastric and intestinal 
antiseptics we have. It has been found that part of the ingested drug 
is excreted by the bronchial mucous membrane and, while it cannot be 
expected to destroy the bacilli in the lungs—hardly any drug could 
reach the avascular tubercle, even if it could be given in sufficiently 
large doses—it is said to exert there a beneficial influence, as is evidenced 
by the decrease in the amount of sputum brought out, and the diminu- 
tion in the intensity of the associated bronchitis, laryngitis, and 
tracheitis. Pharmacological evidence along these lines is, however, 
wanting. Experimental tuberculosis is not at all influenced benefi- 
cially by creosote. Lydia M. DeWitt! and her coworkers have even 
found its bactericidal power very low. 

It is a peculiar fact, not generally appreciated, that creosote often 
provokes general and local reactions which are analogous to those 
provoked by tuberculin. Usually with excessive doses, but occasion- 
ally also with minimal doses, after taking creosote for several days 
the patient is overtaken by a feeling of chilliness and fever, pain in 
limbs, back and joints, weakness, fatigue, and insomnia. Malaise, 
gastric disturbances and even vomiting in patients whose stomachs 
have heretofore not given any trouble, now make their appearance. 
The part of the creosote eliminated through the bronchial mucous 
membrane often excites a focal reaction which, at times, reminds one 
of the focal reaction of tuberculin. Of course, in the case of tuberculin 
a single dose is often enough to produce this reaction, while in the 
case of creosote it is only the more or less prolonged administration 
that is apt to produce this effect. In such cases sanguineous expectora- 
tion and even hemorrhage are not uncommon, while the lesion in the 
lung may be aggravated, or even spread. Rales, which were previously 
absent or scanty, now make their appearance and the general aspect 
of the patient is aggravated. 

If the administration of creosote is persisted in after these symp- 
toms manifest themselves, the condition of the patient may be 
aggravated to an extent as to render the prognosis hopeless in a case 
that previously had a fair outlook. Smoky urine, like that of phenol 
poisoning, is now seen; the patient complains of a taste of creosote in 
his mouth. This may be followed by vertigo, profuse perspiration, 
chilly sensations, and even cyanosis and collapse, as I have seen in 
one case which was greatly relieved by the discontinuance of the drug. 


1 Jour. Infect. Dis., 1920, 27, 115. 


CREOSOTE 751 


Contraindications.— Bearing all this in mind we can say that creosote 
ws contraindicated in all cases in which it provokes gastric disturbances. 
If after taking moderate doses of the drug the appetite does not 
improve, it should be discontinued. It is also contraindicated in all 
febrile cases in which the temperature is 100° F. or more, and also in all 
progressive cases, because they are the ones in which general and local 
reactions are apt to be provoked and spread the lesion in the lungs. 

Patients subject to hemoptysis must not be given any creosote; even 
blood-streaked sputum should serve as a warning for the immediate 
discontinuance of the drug. Moreover, one must not wait for the 
appearance of smoky urine, but carefully watch for albumin which is 
often brought about by creosote. In general, albuminuria is a strong 
contraindication to the administration of creosote. 

Indications.—IJn all incipient cases in which the appetite is poor and 
digestion defective, creosote may be given. With the improvement in the 
nutrition of the patient, owing to cessation of gastric and intestinal 
fermentation, the local condition in the lungs also shows improvement. 
In chronic, sluggish, afebrile cases of tuberculosis, especially those 
characterized by profuse expectoration, creosote is often of immense 
benefit, if rationally administered. In addition to its good effects on 
the gastro-intestinal functions, it also diminishes the amount of 
expectoration, ameliorates the cough, etc., and with the gain in weight 
and comfort, it has an excellent effect on the psychic state of the patient, 
who becomes more encouraged and hopeful. In fibroid phthisis, 
characterized by profuse expectoration of purulent material, provided 
there is no concomitant emphysema, next to the iodides, creosote is 
the best remedy we have. 

Administration.—A good product must be used. Soon after its 
introduction creosote fell into disuse mainly because of the bad quality 
of the product. Good creosote, fit for therapeutic administration, 
must be obtained from the fractional distillation of beech-wood tar. 
The product dispensed in many pharmacies in this country is obtained 
from the distillation of bituminous coal, and contains many impurities 
which are not well tolerated. A good preparation of creosote contains 
25 per cent of guaiacol, but many of the products dispensed under this 
name, even when obtained from beech-wood, contain much less. 

It is best administered in capsules which do away with the dis- 
agreeable odor. Moreover, the mucous membrane of the stomach and 
intestines is not so easily injured by creosote as that of the mouth and 
pharynx, so that the disagreeable local effects are done away with 
through capsules. Some mix it with balsam of tolu, and it is best 
given after meals. Those who cannot swallow capsules may take it 
in this form: 


Ra TeOcO lth iir Tec wteae. btw. 5. o. .) ett. xxx 20) 
Washout Feteyoyssuail 6 Gg ne ee biz 120.0 
M. §8.—Teaspoonful in water three times a day after meals, gradually increasing. 


(02 MEDICINAL TREATMENT 


R— Creosoti, 


Picisliquide radicis . . . . . . «8a gr. xxiv ies 
Alegohnolistabsoles: ase arent tte enter 1) 1220 
Balsam. peruv. } SE (eee Oey; 15.0 
Abie davakeyandsieeyeail 9 5 5 NE 20.0 
Olei terebinth. rectificati. 
eg Hinde LL 2 ee ae eg 129 
M. S.—Three times a day, one > teaspoonful i in milk or water one hour after meals. 
R—Tannini ia) rl aie Noni Odie Sle ales lw ihe Wall LA, 20.0 
Calei phogphorici ee eee ay, 20.0 
Creosoti ; a ee eee Liss 10.0 


M. —Div. in part 40; ft. capsul. 
S.—One capsule three times a day after meals. 


Beverley Robinson has had good results with the following: 


R—Creosoti oo ee) rt ae ee ee ee CUR 0.5 
Glycerint? to oa ae ee ees 25.0 
Spiritus frumenti .. { vtad 5 il} 100.0 


M.8.—Teaspoonful in water three dimes a day after meals. 


This dose may be increased to two or three teaspoonfuls, or, if it is 
desired to increase the creosote, the amount of it may be doubled. 
If the whisky is deemed inadvisable, elixir calisaya or the compound 
tincture of cardamom may be substituted. 

Many have administered creosote by inhalation and have obtained 
good results. In this country, Beverley Robinson introduced this 
method. He recommends equal parts of creosote and alcohol or, when 
there is much irritative cough, equal parts of creosote, alcohol, and 
spirits of chloroform, on the sponge of a perforated zinc inhaler. The 
inhaler should be used frequently, at first for a few minutes, later 
gradually increasing the time until it is used from half an hour to an 
hour at a time, and finally it may be used almost continually during 
the day and frequently all night. These inhalations have a salutary 
psychic effect on some patients who feel that something is being done 
for them and the odor of the substance impresses even those around 
the patient that an effective remedy is administered. 

The following are good formule for inhalation: 


R—Creosoti a ee Se one ae ot ee oho V IY 0.5 
Tincturse benzoini comp: : ap Pe oat 100.0 
M.S8.—To inhale a teaspoonful from boiling water, three or four times a day; shake. 


R—Creosoti es ON ene eee. CURVED OFS 
Oleipind ‘silvestris = ae ene ene en LSS 10.0 
Oleisterebinthinss saan ee enn ne 1S 5.0 
Tincturze benzoini comp. : Ziv 100.0 


M.8.—Shake. To inhale ate aepoontal tro boiling water, three or four times a day. 


Derivatives of Creosote —Because of its caustic taste, and disagree- 
able odor, creosote is not well tolerated by many patients; even when 
given in capsules the odor is often penetrating. CGuaiacol, the main 
active principle of creosote, can be given instead, but it is msoluble 
in water, has an objectionable odor and taste and is a gastric irritant, 


CREOSOTE 753 


There have been brought out a large number of preparations which 
retain most, or all, of the useful qualities of creosote without its draw- 
backs. These derivatives of creosote are mostly used at present with 
the same result as with the original drug. 

Of these creosote carbonate (creosotal) is perhaps the best. When 
ingested it breaks up slowly in the intestine, liberating creosote. It 
may be given in capsules of 5 to 10 drops three or four times a day. 
Many pharmaceutical houses market globules which are very elegant. 
It may also be given to patients to be taken in a certain number of 
drops in water, milk, or coffee; or the following prescription is useful: 


he @reosourcarbonatist mia) es soe eo ee) Slv 120.0 
PS CnerIS ee eee ae eye eb. Sey) a) gtk Moe S188 5.0 
FAT CONOMS: SO] GmetEua: ae el SU cake VY 25.0 
‘Vier tines a ns gtt. vij 0.5 


M.S8.—Fifteen drops in water or in 7 mille three times a day after meals; increased if 
well tolerated. 


In many cases between 30 and 60 grains of creosote carbonate may 
be given per day. Guaiacol carbonate (duotal) is another preparation 
which is very extensively used. It may be given in powder or capsule 
from 10 to 30 grains a day, or combined with arsenic. 

Both of the above preparations are now sold quite reasonably. 
But for those who can afford to pay, we have a wider range of choice. 
Styracol (guaiacol cinnamate) contains a high percentage of guaiacol. 
Thiocol (potassium- -guaiacol-sulphonate) may be given in 5 to 15 
grains three times a day in powder, tablet, or eapsule It is a non- 
toxic, tasteless, odorless powder, soluble in water. Many patients 
who do not tolerate guaiacol take this preparation very well, and in 
those who suffer from diarrhea it is to be preferred. But it contains 
less guaiacol than most other preparations of this class and its action 
is not so intense as that of the others. In fact, it is sometimes not 
decomposed in the intestines, and may be excreted unchanged. For 
those who prefer their medicine in liquid form and for children, it may 
be given in the form of sirolin, a 10 per cent solution of thiocol in 
orange syrup, which may be given one to three teaspoonfuls three 
times a day. There is no doubt that many who cannot tolerate 
creosote or guaiacol take this less toxic preparation very well. 

Sir R. Douglas Powell recommends the following: 


R—Guaiacol carbonatis, guaiacol benzoatis vel styracol 3iss 6.0 
GalcionypOoOlOspoa tion menue a. eg 0 we 2h 58S 2.0 
Palvis tragscauthse comps =| <.) 5 +. «=. « Od 4.0 

Misce bene, adde guttatim: 

Syr. pruni virginiane vel elixir aurantii . . . jss 16.0 
Syr. calcii Pr OLOrHeEs vel syr. hy Rophovohs; 

KUIT GON Dew eet tee eens eee Oo 32.0 
Aquse chloroformi. . Tadeo Vy 190.0 

S.—One teaspoonful in sey or Tauid malt three times a day soon after meals. 

R=-Grevsotlcarbonatist “1) S) a8 <2 a sf. solv 16.0 
Tinct. gentian COMME Ge & Aerie ery Sys Biv 16.0 
Syr. pruni virginianse gg Niece 11) 90.0 


S.—One teaspoonful in a wineglass of ive or rma extract after meals three times a 
day. Increase the dose by five drops each second day up to two teaspoonfuls by measure. 


48 


154 MEDICINAL TREATMENT 


Ichthyol.— Ammonium sulphoichthyolate or ichthyol has been found 
very useful in many cases of phthisis. Some authors state that it has 
a favorable influence on the metabolism, prevents albuminous decom- 
position and favors assimilation of food. Helmers found that about 
one-third of the sulphur ingested with ichthyol circulates in the 
juices of the body; others asserted that it even has a bactericidal 
action, without hurting the body cells, etc. It may, however, be stated 
that we do not know the exact pharmacology of this preparation, but 
that empirically it has been found useful in many cases of phthisis. 

It may be given in water 2 to 5 drops three times a day, beginning 
with the smaller dose and gradually increasing according to tolerance. 
Because of its disagreeable odor and taste, the drops should be diluted 
in large quantities of water or milk and given before meals. It may 
also be administered in black coffee. Or the following formule may 
be used: 


R—Ichthyolisi\ 4) aa wet yy eee ee > a eee eo day UY, 
Aquse distil: (225 5 9 ete ee ee 60.0 
Alcoholis'rectiics 20 —) See) ata a rn] €0.0 
Syr. citr., 

Syr. aurant cort . ee Heh 3iss 50.0 


M. 8.—Teaspoonful in erator Prac Limes a day before meals. 


De Renzi says that the above formula conceals the taste and odor 
of ichthyol. The following is also of use: 


R—Ichthyolis* ¢ 27s os. 1 Pho (ae en ee eS 10.0 
Syrup simples. (2. “Pe ee oe ee 20.0 
Aque menth. piper. . 3 ij 80.0 


M. 8.—Teaspoonful in a glaas of w ater these times a day. 


In many cases ichthyol improves the appetite, diminishes the fre- 
quency of the cough and the expectoration, changing the latter so that 
its purulent character vanishes. The general condition of the patient 
improves with the improvement in the nutrition. In some patients 
the remedy disagrees, causing flatulence, abdominal pains, diarrhea, 
loss of appetite, and eructation of gases. In fact, as has been shown 
by Barnes, in patients in whom the administration of ichthyol does 
not immediately improve the appetite, it is not advisable to continue 
the drug. I can add that diarrhea also shows that the drug disagrees. 
My patients do not, as a rule, mind the disagreeable odor and taste 
when given well diluted with water, milk, or coffee. 

Ichthyol should be tried in every case of phthisis because it has 
not the dangerous characters of creosote and arsenic and their deriva- 
tives; in fact, it is well tolerated in most cases, only gastro-intestinal 
disturbances occasionally preventing its use. 

Arsenic.— For centuries arsenic has been used by physicians in the 
treatment of tuberculosis. As has been pointed out by A. Arkin and 
H. J, Corper,! Dioscorides employed it internally and by inhalation. 


+ Jour, Infect, Dis,, 1916, 18, 335, 


ARSENIC 755 


Antylus, who lived in the third century 4.p., Marcellus Empyricus, 
and Galen all recommended it and described cures from the inhalation 
of powdered arsenic. The Chinese and the Hindus also found it useful 
in tuberculosis. Empirically, it has also been employed by modern 
physicians in various forms, and many report excellent results. While 
some claimed that it has a direct action on the tubercle bacilli, recent 
careful investigations by Arkin and Corper have shown that this is 
not the case. Many preparations of arsenic—sodium arsenite, sodium 
cacodylate, mercury cacodylate, atoxyl, arsacetin, and neoarsphen- 
amine have all been found without any action on tubercle bacilli zn vitro. 
Administered to tuberculous animals parenterally these preparations 
of arsenic were subsequently found in the liver, lungs, kidneys, blood, 
spleen, and tuberculous tissues (lymph glands of guinea-pigs and eye 
of rabbit), the concentrations in all these tissues not greatly differing. 
No evidence of accumulation in the tuberculous tissues was obtained 
thus showing that it has no selective affinity for tubercle. 

Clinical experience has, however, shown that arsenic is an excellent 
stimulant of nutrition, a hematinic, reconstructive, and alterative in 
chronic wasting diseases, including phthisis. The various organic 
arsenic compounds recently introduced were stated to lack the greater 
part of the toxicity of arsenic, while retaining its curative, reconstruc- 
tive, and antiseptic properties. ‘The advocates of arsenic medication 
in tuberculosis claim that it increases the appetite, improves assimila- 
tion of food, and stimulates the blood-forming organs, in addition to 
its stimulating effects on the nervous system. In short, arsenic is sup- 
posed to fortify the tissues against the ravages of the tubercle bacilli. 

From an extensive use of arsenic in phthisis the author has not 
found that it exerts any direct influence on the tuberculous lesion in 
the lungs, even when administered to patients who tolerate it. The 
quantity and quality of the expectoration are, however, very favor- 
ably influenced in some cases; purulent sputum often becoming mucous 
and greatly reduced in quantity. With the improvement in the appe- 
tite and nutrition a great deal is gained—the patient is encouraged. 
The fever is, however, not influenced, nor are the nightsweats. In 
fact, it should not be given to febrile patients. 

It may be given as an adjuvant to creosote treatment in the form 
of trioxide, as in the following formula: 


R—Gualacoliscarbonatis. . . . . .. . . 3V 20.0 
PXRSen GlctriO KIC kame ann ae meee oe ee eee) or? sg Veal 
SErycnminesrsulphatigeae seule.) wh als Ve. oral 0.06 


M.—Ft. pilule no. Ix div. 
S.—One pill three times a day after meals. 


It may be given in the form of Fowler’s solution, beginning with 2 
or 3 drops after meals and increasing daily until 10 drops are taken 
three times a day. . 

During recent years various organic compounds of arsenic have been 
used in phthisis, administered either by mouth or hypodermically. 


756 MEDICINAL TREATMENT 


Of these the cacodylates of sodium, strychnine, iron, and guaiacol may 
be mentioned. Many of these, as well as atoxyl, are at present sold 
by pharmaceutical houses in ampoules ready for hypodermic and 
intravenous administration. But in my experience none of these 
preparations has any advantages over the inorganic arsenic; the 
trioxide, and Fowler’s solution, answer all requirements. In fact, some 
of them, notably atoxyl, are dangerous because they are liable to 
cause amblyopia. Attempts at utilizing arsphenamine in the treat- 
ment of phthisis have met with failure to observe beneficial therapeutic 
effects, excepting in tuberculous patients who also have syphilitic 
lesions. 

When administering arsenic to phthisical patients certain precau- 
tions are to be taken. It should not be continued, especially in large 
doses, for more than a week or ten days. Symptoms of intolerance 
may make their appearance, such as loss of appetite, thirst, and dryness 
in the mouth, colicky pains, and diarrhea. In some cases the fever 
rises as a result of large, or even small, doses of arsenic. Tachycardia, 
cardiac palpitation, and insomnia are occasionally observed. It should 
not be given to febrile patients, and to those showing a tendency to 
hemoptysis. In fact, if during the administration of arsenic there 
appears streaky sputum, it should be considered a danger signal and 
the arsenic is to be discontinued at once. 

Iodine.—I*or generations iodine has been used in the treatment of 
scrofulous children with good results. It has also been found useful 
in assisting the resolution of pleural adhesions, and in the relief of the 
symptoms of chronic bronchitis, pulmonary emphysema, and asthma. 
That the iodides have an effect on tuberculous lesions in the lungs is 
evidenced by the fact that small doses of the iodide of potassium 
may cause, In persons with incipient tuberculosis, reactions similar 
to those produced by tuberculin, as was shown by Rondot. In fact, 
many authors recommend it for diagnostic purposes, at least to pro- 
voke expectoration which may be examined for tubercle bacilli. Sorel! 
found that tuberculous animals, when given large doses of potassium 
iodide, succumb to generalized miliary tuberculosis, and usually much 
earlier than the controls. 

Recent investigations tend to show that iodine counteracts and 
inhibits the lipoid element in the tubercle bacilli. Joblings and Petersen 
found that soaps of the unsaturated fatty acids were capable of inhibit- 
ing the action of trypsin and other ferments, and, moreover, they 
discovered in the tubercle bacilli a ferment inhibiting substance of the 
nature of a lipoid, to which they attribute the lack of autolysis and 
consequent caseation in tuberculosis. They found that the higher 
the iodine value of a soap the less was its activity as an inhibiting 
agent, while saturation with iodine would destroy entirely its inhibiting 
powers. They also found that ether-soluble substances of the bacilli, 


1 Ann. de l'Inst. Pasteur, 1909, 23, 533. 


= 


MERCURY 757 


which constitute 25 to 35 per cent of their weight, and which are 
largely composed of fatty acids, have a marked restraining action 
ontrypsin. It is thus suggested by E. Curtin that iodine acts in tuber- 
culosis by saturating the unsaturated bonds of the fatty acids of the 
lipoids, rendering the substituted product less active as an anti- 
tryptic agent. 

Some French authors recommend the iodides in most cases of pul- 
monary tuberculosis, but it seems to be a dangerous drug for the 
reasons just stated. But in some cases of incipient phthisis without 
fever the iodides do good, especially in those in whom the tuberculous 
process has been implanted on emphysematous lungs. This is also 
true of asthma and tuberculosis—the iodides often control or relieve 
the nocturnal attacks of dyspnea. But one must always guard against 
giving this drug to sufferers from the congestive, inflammatory, pro- 
gressive lesions, and those subject to hemoptysis. 

It is best given ina saturated solution of iodide of potassium of which 
each drop represents | grain of the drug. Small doses are to be given 
at first, 2 to 5 grains, three to five times a day. If no intolerance is 
shown it may be increased. I have often used some of the organic 
compounds of iodine—sajodin, ete.—with good results. 

A better way of administering iodine is giving the pharmacopeial 
tincture in increasing doses, beginning with one drop well diluted 
in water or milk, three times a day, and increasing daily by one drop, 
until twenty or even thirty drops are given daily, or until toleration 
is reached. Some patients show symptoms of iodism very soon, and 
the dose must be reduced, but in the majority of cases large doses may 
thus be given for a long period with very marked results. In fibroid 
phthisis it has often proved invaluable. 

Mercury.— Mercury has been used in the treatment of tuberculosis 
for many years. But more recently Dr. B. L. Wright developed a new 
method of administering it and reported a larger number of recoveries 
than has been claimed with any other medication. He used the 
succinimide of mercury hypodermically, in doses of 4 of a grain given 
on alternate days, increasing the dose guardedly until the limits of 
toleration are reached. As soon as symptoms of mercurialization 
appear, or there is a rise in the temperature, anorexia, loss in weight, 
etc., the dose is either reduced or the treatment is discont_nued for a 
time. In most cases about thirty injections are given, followed by a 
rest of two weeks, during which period iodide of potassium may be 
administered. A second ser'es of injections is given to those who 
tolerate the drug. 

I have tried this treatment and found it of immense value in phthisis 
complicating syphilis; otherwise it is decidedly harmful. As was 
already stated, it appears that when tuberculosis is implanted in 
a syphilitic subject, the disease is apt to run a very sluggish, chronic 
course. Fibrosis is very active. In these cases both the iodides and 
mercury, if intelligently and guardedly administered, may be very 


758 MEDICINAL TREATMENT 


efficacious. The succinimide of mercury may be used instead of 
other forms of the drug. But the doses given by Wright are decidedly 
excessive—the same results may be obtained by the hypodermic 
administration of ¢ or 3; of a grain twice weekly. On the other 
hand, arsphenamine now offers a better means of combating active 
syphilis combined with tuberculosis than the succinimide of mercury. 

Hypophosphites and Glycerophosphates.—It will be noted that 
most of the medicinal preparations mentioned above have their indi- 
cations and contraindications, and some are not without danger when 
improperly administered. The safest medication in phthisis appears 
to be the time-honored administration of the hypophosphites. Re- 
cently the glycerophosphates of lime, iron, magnesium, etc., have 
been used very extensively on the theory that phthisis is a manifes- 
tation of lime starvation and that recalcification and remineralization 
of the body are of great importance in our efforts at combating the 
effects of the tuberculous process. There is no doubt that in many 
cases of phthisis these medicinal substances have an excellent influence 
on the nutrition of the patient and they are also of use in relieving 
the anemia which is such a frequent accompaniment of the disease. 
We may give the official compound syrup of hypophosphites in doses 
of one to two teaspoonfuls three times a day after meals. The glycero- 
phosphates may be given in any form. Pharmaceutical houses have 
many elegant and palatable preparations of glycerophosphates in 
tablet, capsule, and liquid forms which may be used. Their onic 
effects are beyond question. 

Cod-liver Oil.— Physicians of past generations bestowed great 
confidence in the therapeutic virtues of cod-liver oil in tuberculosis, 
and many modern practitioners still consider it an excellent therapeutic 
agent. Some have ascribed the curative action of this oil to certain 
of its constituents. Thus, some believe that it is the iodine which 
is effective, others see in the bromine the active principle. But careful 
chemical analysis has shown that there are only traces of these elements 
in cod-liver oil. The biliary salts, the hepatic ferments, the lipoids, 
the lecithin, etc., have been stated to be of more value than the fat 
of cod-liver oil. John W. Wells,! and others believe that, in addition 
to the ready absorption of the fat of cod-liver oil, it possesses powers of 
increasing the absorption of other fats of the food to a marked degree. 

The recent intensive studies of the internal secretions have also 
thrown some light on the action of cod-liver oil in phthisis, according 
to some authors. Thus, Williams? stated that the superiority of 
this oil to others is mainly due to the internal secretion of the liver 
of the fish, which “when introduced into the human economy, acts 
as a stimulant to one of the normal internal secretory glands, and 
the secretion of the one so stimulated is inimical to the development 
of the tubercle bacilli.’ He believes that only the crude oil contains 


1 British Med. Jour., 1902, 2, 1222. 
2 Practitioner, 1911, 88, 605. 


COD-LIVER OIL 759 


these active principles and is therefore more efficacious than the 
refined oil. Iscovesco,! from his experimental researches, is con- 
vinced that the efficaciousness of cod-liver oil is due to the lecithides 
which it contains. He treated a large series of animals for four months. 
Those which got cod-liver oil increased in weight to the extent of 55 
per cent; those which got cod-liver oil from which the lecithides had 
been removed gained only 27 per cent; those who were given olive 
oil gained 33 per cent; others were given oil to which was added 0.5 
pro mille of the lecithides extracted from cod-liver oil and they gained 
56 per cent. The control animals gained only 29 per cent. Williams 
and Forsyth? claim that the unsaturated fatty acids of cod-liver oil 
tend to disintegrate the waxy envelope of the tubercle bacilli, thus 
destroying them. 

These theories are interesting, and deserve further study, but there 
is no doubt that cod-liver oil is an important remedy in tuberculosis, 
even if only for the fact that it contains a considerable proportion of 
easily assimilable fat, and it may be used as a food rather than as a 
drug. Patients who do not take such animal fats as butter, etc., are 
distinctly benefited by cod-liver oil. 

Cod-liver oil should be given in large doses; to some patients as 
much as 2 ounces per day may be given and some French authors, like 
Jaccound, Grancher, and Daremberg, have given more than 4 ounces 
per day. Some apparently have a marked tolerance for this prepara- 
tion, and they may utilize it instead of superalimentation. On the 
other hand, there are patients who cannot tolerate it, and even small 
doses cause eructations, nausea, and oily taste in the mouth. Diarrhea 
is another of the untoward effects in some who do not bear the oil 
very well. 

Indications. —Cod-liver oil is indicated in all afebrile cases of phthisis. 
All patients who willingly take it and digest it well in large doses 
should be given this oil, without incidentally curtailing their usual 
amount of other nourishment. It may be continued for a long period 
of time; as long as the patient is apparently benefited by it and his 
digestive functions remain normal, the appetite is good and, above 
all, there is no diarrhea. Patients with fever do not tolerate it as 
well as those who have no pyrexia. Children with tendencies to 
scrofula, with enlarged tuberculous glands, especially tracheobronchial 
adenopathy, and who are as a result underfed and anemic, often 
derive great benefit from cod-liver oil. It appears that children take 
it with greater ease, and more often with distinct benefit, than adults. 

Contraindications.—Cod-liver oil is contraindicated in cases in 
which the patients do not tolerate it in even small doses. The best 
criteria are the state of the appetite and digestion. As soon as these 
are deranged, it should be discontinued. 


1 Compt. rend. Soe. de biol., 1914, 76, 34. 
2 British Med. Jour., 1909, 2, 1120. 


760 MEDICINAL TREATMENT 


Administration.—So long as we consider cod-liver oil merely a fat 
food, and disregard its other constituents, it is best to administer it 
in as palatable a form as possible. In former times the crude oil, a 
product of decomposition of the livers of the cod, was used. Some 
modern authors even now insist that this form is most beneficial for 
phthisical patients. But it has a very disagreeable odor and taste and 
it requires courage on the part of the patient to swallow it. It is also 
apt to cause indigestion, eructations, diarrhea, etc. The light, or 
amber-colored oil, prepared by melting fresh livers by a steam process, 
is less disagreeable and more easily tolerated. It should at first be 
given in small doses of the Norwegian, light-colored oil, and in case 
the gastro-intestinal tract tolerates it, the dose is to be increased so 
that within a few weeks the patient takes four to six tablespoonfuls 
a day after meals. It should not be forced on patients; when they 
refuse to take it, or if it causes nausea, eructations, diarrhea, etc., it 
should be discontinued. 

It is best that the pure oil should be given and many patients take 
it easily. With some the odor and taste have to be masked, and this 
may be done in the following manner: It may be given in orange- 
juice, or in some volatile oil. Many patients take it with ease in coffee 
ormilk. A pinch of salt placed in the mouth before taking it may dis- 
guise the taste. Those who are allowed to take alcohol may take 
some whisky or brandy into the mouth where it is kept for a few 
seconds without swallowing, and then the oil is taken. Some use 
peppermint-water or tomato ketchup for the purpose, or orange- or 
lemon-juice. The difficulties owing to the odor and taste are over- 
come soon in most patients, and they take it freely. 

The various emulsions offer no advantage over the pure oil. If 
they contain the indicated percentage of the oil, they are as dis- 
agreeable as the pure article, and one who can take an emulsion can 
take and digest the oil. The various preparations and “extracts” 
which are alleged to have all the therapeutic qualities of cod-liver 
oil without any of its disadvantages, have been found worthless, 
lacking as they do the fatty substances which are of value for the 
nutrition of the patient. On the other hand, many of the preparations 
of cod-liver oil and malt, hypophosphites, creosote, etc., may be 
utilized in the treatment of phthisis with advantage. It is, however, 
to be borne in mind that large doses are necessary to procure results, 
and that these preparations contain but a small proportion of cod- 
liver oil. 


CHESPr Rew ULI: 
SPECIFIC TREATMENT. 


STRICTLY speaking, the term “specific”? should only be applied to 
a remedy or preparation which has a proved selective curative effect 
on a certain disease. From this viewpoint we can state wnequivo- 
cally that we have no specific remedy for tuberculosis in any of its clinical 
forms. We have no substance, drug, or preparation which will cure, 
or remove, or ameliorate the symptoms in the vast majority of 
phthisical patients to the same degree as mercury or arsphenamine is 
efficacious in syphilis, quinine in malaria, or thyroid in myxedema. This 
is a fact which all thoughtful workers in the tuberculosis field acknowl- 
edge; even those who employ tuberculin extensively, and do not hesi- 
tate to call it specific treatment, say that it is only a good adjuvant 
to other therapeutic methods which should be tried in selected cases 
so long as a true specific is not available. Moreover, it appears that 
tuberculin only works in sanatoriums, where the patients are, in 
addition to the specific treatment, subjected to a rigorous hygienic 
and dietetic regimen. It is distinctly stated that when the latter is 
lacking, tuberculin is of no avail. 

It appears that the only justification for the use of the term specific 
when speaking of tuberculin treatment is the fact that this word has 
recently received a wider application and is now also used to designate 
remedies which are especially indicated, and used, in any particular 
disease. 

The writer has given tuberculin therapy a fair trial in both his 
hospital and private practice and found it either altogether wanting 
in therapeutic effects when used in infinitesimally small doses, as is 
advised by most of its contemporary advocates, or decidedly harmful 
when given in substantial doses. This opinion is shared by most of 
those engaged in the treatment of tuberculosis, excepting such as 
have themselves discovered some tuberculin, or who are in charge 
of sanatoriums catering to well-to-do private patients. In the public 
sanatoriums in this country very little of tuberculin is used for thera- 
peutic purposes. The vast majority of patients in these institutions 
are cared for by the old methods. It cannot be said that it is the 
cost which precludes the use of tuberculin in public institutions. 
Arsphenamine is a really expensive drug but is used in all hospitals. 

Our reasons for discarding tuberculin from the therapeutic arma- 
mentarium are the following: 

The Variety of Tuberculins.—It is an old axiom in therapeutics 
that the larger the number of drugs recommended for any given disease, 
the less the chances of curing it with any of those mentioned as effica- 


762 SPECIFIC TREATMENT 


cious. Thus, we have only to consult the index of any standard materia 
medica and count the number of remedies recommended for typhoid 
fever, pneumonia, nephritis, gastritis, etc., and to compare it with 
the number mentioned as effective in myxedema, malaria, syphilis, 
valvular heart disease, etc., to be convinced that the axiom holds 
good. ‘The large number of tuberculins alone should give us a strong 
hint that none of them is a specific, or will surely cure. I counted in 
one German book forty-six varieties of tuberculins, and I could add 
almost as many which the author has not mentioned. 

“We have no standard tuberculin,” says William Charles White,! 
himself an advocate of tuberculin, “‘and furthermore we have no 
manufacturer who prepares the same strength twice. Consequently 
the dose of one tuberculin is no more the dose of another tuberculin 
than the dose of a sherry glass is the dose of a champagne glass. We 
have no method of testing the strength of a given tuberculin unless 
it is the biological one, and this is tedious, if it has to be used for 
every patient for every new supply of tuberculin. If, however, the 
tuberculin standard is at fault, what a vastly greater difference exists 
in the physicians who administer it? There are almost as many 
methods of dosage and administration as there are administrators. 
Zach physician believes his method the best. Some have no method 
at all.” It appears that for practical purposes we have no methods 
to weigh or measure the toxicity of tuberculins. Two preparations 
made by the identical method may differ very much if they are derived 
from different cultures; especially do they vary with the age of the 
culture. 

All authors entitled to an opinion agree that the action of all tuber- 
culins is the same. The preparations differ only as regards their 
strength, toxicity, capacity for absorption, etc. But tmasmuch as 
the active element or substance of tuberculin has not yet been isolated, 
nor can the strength of a given preparation be measured, it appears 
that the differences which are known to exist between the various 
forms of tuberculin cannot be definitely ascertained. Arsphenamine 
strychnine, morphine, digitalis, or tetanus and diphtheria antitoxin 
which could not be measured would hardly be used by medical men. 

In general it may be stated that there are three varieties or types 
of tuberculin: 

1. Old tuberculin, consisting of the exotoxin—a glycerin extract 
containing the soluble products of the tubercle bacilli in the medium 
in which they have grown, glycerin, bouillon, extractives, etc. Though 
it should be mentioned that most investigators are of the opinion that 
there is no tuberculous exotoxin. 

2. The new tuberculins, made up of the insoluble endoplasm of the 
bacilli and the poisons contained within them—endotoxins. 

3. Those which consist in a mixture of both the above forms. 


1 Tr. Fifth Annual Conference Nat. Assn. Prevent. Consumption, London, 1913, p. 70. 


ACTION OF TUBERCULIN 763 


But when injected into the tuberculous human or animal body any 
tuberculin produces practically the same effect. On this nearly all 
agree, even those who maintain that only a certain variety of tuber- 
culin should be used if therapeutic results are to be obtained. 

Action of Tuberculin.—As was already stated (see p. 37), tuber- 
culin is harmless when injected into a non-tuberculous body, and pro- 
duces its toxic effects only in those who have suffered a tuberculous 
infection. But we do not know how it acts under these circumstances. 
Wolff-Eisner’s tuberculolysin hypothesis is about the most plausible 
and the one accepted by most authors. But we have not as yet 
succeeded in isolating a specific tuberculous antibody, nor the tuber- 
culolysin from the serum of infected animals. 

At first sight it would appear that tuberculin is specific, considering 
that it acts only on infected organisms, but even this is not conclusive. 
It seems that the infected organism is not only hypersensitive to 
tuberculin, but to all foreign proteins. We can produce elevation of 
temperature, malaise, backache, nausea, etc., and even the local 
reaction, by the injection of any foreign protein into a tuberculous 
person. ‘‘Neither the local nor the general reaction is absolutely 
specific,” says Baldwin,! himself using tuberculin extensively; “ vari- 
ous nucleoproteins, yeast nuclein, bacterial proteids in general, and 
digestive products, such as albumoses, are capable of producing similar 
effects. Cinnamic acid, cantharidin, pilocarpin, and other alkaloids 
also act to some degree, although less as local irritants than general 
leukocyte stimulants.” Parenteral milk injections have also been 
found to produce general and local effects not unlike those of tuberculin. 
In my experience, potassium iodide and creosote, when given in large 
doses, may produce general and focal reactions not unlike those pro- 
duced by tuberculin. 

All efforts at producing partial or complete immunity with the 
administration of tuberculin in man or animals have utterly failed. 
Even Sahli, who urges tuberculin treatment, says that “tuberculin 
treatment has not the character of a true immunization, though it 
produces immunizatory effects in the organism.” 

That it is not necessarily the reaction which is effective thera- 
peutically is clear when we consider that modern tuberculin treatment 
aims at eliminating entirely these reactions by the administration 
of infinitesimally small doses. The hope that the focal reactions, 
consisting in hyperemia at the site of the lesion, and the surrounding 
tissues, may promote the healing of the lesion, cannot be seriously 
entertained by clinicians. Usually when the focal reaction is intense, 
it cannot be controlled and the congestion often produces renewed 
activity of the diseased process. Quiescent foci, calcareous particles, 
are “‘sleeping dogs” and should not be disturbed, as Sir James Kk. 
Fowler? says. The establishment of tuberculin tolerance, which some 


1 Osler’s Modern Medicine, 1, 308. 
2 Tr. Annual Conference Nat. Assn. Prevent. Consumption, London, 1918, 5, 98. 


764 SPECIFIC TREATMENT 


strive at, is no proof of healing; in fact, it is usually short-lived. More- 
over, the tuberculin reaction is a very complex process and varies 
with the preparation used, the individual treated and also with the 
time it is administered. One day the patient is tolerant, the other he 
is badly affected with even a minimal dose. 

There is no harm in administering most drugs in teaspoonfuls, 
tablespoonfuls, or measuring them with the point of a knife, as has been 
done for centuries. Patients have recovered with such inexact meas- 
ures, some may have been harmed, but lethal doses are rarely given 
in this manner. But we cannot give a potent agent like tuberculin 
to a patient who needs all the vital energy he has, and more, in this 
manner, any more than we can give with impunity strychnine, mor- 
phine, digitalis, arsphenamine, etc., without exact dosage. So long as 
we cannot measure the toxicity of tuberculin, we cannot administer it 
rationally and prevent sudden and at times harmful, reactions which 
may appear when least expected. 

Experimental Evidence of the Lack of Therapeutic Effects of Tuber- 
culin.—'Tuberculin as a therapeutic agent is based on results obtained 
in the laboratory through animal experimentation. It would be 
reasonable to exact that it should be efficacious in experimental tuber- 
culosis in animals. But it is a fact that there is no record in medical 
literature that any investigator has succeeded in curing or benefiting 
a tuberculous animal with tuberculin treatment. In Robert Koch’s 
writings at the time he introduced tuberculin we can find no clear-cut 
statement to the effect that he cured an animal with this agent. 
Klimmer, Lydia Rabinowitsch,! and others have recently tried small, 
very small doses, corresponding to those used at present in the treat- 
ment of human phthisis, but the tuberculous guinea-pigs and rabbits 
failed to improve. “No curative influence has been exercised by the 
tuberculin. ‘The control animals lived sometimes longer than the 
treated animals. On the use of large doses the animals readily suc- 
cumbed.”’ 

It has never been observed that the administration of tuberculin to 
tuberculous animals should promote healing of a tuberculous lesion, 
that cicatrization should be favored. 

What has been observed, however, is that very often dormant tuber- 
culous processes are activated after the administration of tuberculin. 
Bacilli which gave no trouble were released, “‘mobilized,” producing a 
bacteremia, as was already mentioned (see p. 284). 

Serologically, tuberculin has hardly ever shown its therapeutic 
value. Like other antigens, tuberculin stimulates the production of 
antibodies when inoculated into a tuberculous organism. But these 
antibodies cannot be considered true antituberculins because they do 
not neutralize tuberculin in vitro. We know that the antibodies pro- 
duced by other toxins, as those of tetanus and diphtheria, neutralize 


1 Tr. Annual Conference Nat. Assn. Prevent. Consumption, London, 1913, p. 44. 


CLINICAL EVIDENCE 765 


the toxins of these infections in vitro, while the tuberculous antibodies 
do nothing of the kind. We can consequently see no theoretical or 
practical value in tuberculin from this viewpoint. 

Clinical Evidence.—In a discussion on the merits of tuberculin treat- 
ment, Hector W. G. Mackenzie! said that “he should like to ask 
whether anyone has been able to obtain a cure of tuberculous ulcer, 
arising from the primary inoculation by means of tuberculin injections. 
He fears the answer must be in the negative.”’ 

We arrive at the same conclusion when we consider the clinical 
evidence presented by the advocates of tuberculin treatment in phthisis. 
All effective medication has its indications, contraindications, and 
limitations. ‘True specific treatment is not free from these limita- 
tions, as is true of quinine, mercury, arsphenamine, thyroid, ete. But 
the limitations in the range of usefulness of these drugs depend mainly, 
if not entirely, on the presence or absence of mixed infection, of pre- 
existing diseases, on the constitutional peculiarities of the patient, 
and complicating diseases. In a clear-cut case of syphilis in the 
average patient, arsphenamine or mercury will produce evident curative 
effects; malarial fever will be abated by quinine, myxedema is relieved 
by thyroid, etc. But in the purest forms of tuberculosis, in acute 
miliary tuberculosis, tuberculin is powerless, which fact alone should 
arouse suspicion as to its specific qualities. 

It appears to be a general rule in pathology, as has been pointed 
out by von Hansemann,’ that diseases which are not at times spon- 
taneously cured cannot be cured by any known therapeutic measure. 
Rabies is usually mentioned as an exception, but even this may only 
be prevented; once it has developed, it cannot be cured. Specific 
therapeutics aims at curing diseases which are not known to be cured 
spontaneously. But it has never been observed that a patient suffer- 
ing from acute miliary tuberculosis should be cured, the few cases 
mentioned by Cornet are all very doubtful. Acute miliary tubercu- 
losis is the purest form of the disease without mixed infection; the 
tubercle bacilli, though disseminated all over the body, are found in 
each place in small numbers and they do not produce avascular masses 
from which medication is excluded. It should be the crucial test for 
specific treatment. As a matter of fact, however, tuberculin is alto- 
gether powerless in acute miliary tuberculosis, as it is in all progressive 
cases of phthisis. 

Good results are reported by those who have used it in glandular, 
osseous, and articular tuberculosis in children. But we have already 
mentioned that these have a strong natural tendency to heal spon- 
taneously in the vast majority of cases (see p. 471). Even surgeons 
advise and practise conservative treatment. 

In phthisis the ideal cases are said to be those in the incipient stage 
of the disease. But when we recall that a really incipient case is one 
which has “slight or no constitutional symptoms, including particularly 


1 Tr. Annual Conference Nat. Assn. Prevent. Consumption, London, 1913, p. 9. 
2 Berl. klin. Wehnschr., 1911, 47, 1. 


766 SPECIFIC TREATMENT 


gastric or intestinal disturbances or rapid loss of weight; slight or no 
elevation of temperature or acceleration of pulse at any time during 
the twenty-four hours,”’ we are not surprised that many recover with 
tuberculin treatment. It was found that in Germany, France, and 
England many of those who were certified as tuberculous and eligible 
for sanatoriums, were fit for military service. Instead of sending them 
to institutions, as was the rule during times of peace, they were sent to 
the trenches and in the vast majority of cases they stood the hardships 
of war as well as other soldiers. Evidently many cases are abortive 
tuberculosis which under ordinary circumstances pass as chronic 
phthisis and any form of treatment gets credit for a cure. ‘Tuberculin 
evidently gets its share of credit. 

Lack of Reliable Statistics of the Efficacy of Tuberculin.—'l’o prove 
its therapeutic efficacy, a specific must produce results in a larger 
proportion of cases of phthisis than is observed with the older methods 
of treatment. This has not been shown. In fact, there are no reliable 
statistics of large series of cases available. In their book on tuber- 
culin treatment, Riviere and Morland state that they decided to 
give no statistics of results of tuberculin treatment, because they 
consider figures of questionable value. Sahli also gives no statistics, 
while the figures compiled by Brown in Klebs’s book show clearly that 
there was no difference in results between the group treated with, as 
compared with those treated without tuberculin. Reliable statistics 
of ultimate result are not available at all. 

Dosage.—It would be pretty bad for physicians, and for patients, 
if there was such a disagreement as to the dose of any potent remedy, 
especially if it was not known which quantity of the remedy is likely 
to be harmful. The initial dose ranges between 1 mg., recommended 
by Bandelier and Répke, to 0.0000005 mg., recommended by Philippi. 
Between these two extremes, various authors recommend intermediate 
quantities, each one claiming that his standard is best, or, what is of 
more importance, the safest. Still, with such uncertainty as to dosage, 
many authors make tables of dosage and iron-clad rules as to gradual 
increase in the dose, and the final dose, some using logarithmic tables 
for their calculations, as if they were dealing with an exact science. 

The fact is that there is no mystery about the technic of adminis- 
tration of tuberculin, and no knowledge of higher mathematics is 
necessary to make the various dilutions properly. Many pharmaceuti- 
cal houses sell tuberculin in proper dilutions ready for use. But those 
who want to make their own dilutions can do it easily. 

All that is necessary is six or ten amber-colored bottles of 10 or 20 
ee capacity each. They are to be clean and properly sterilized. A 
larger bottle containing the diluent (sterilized, or distilled water 
containing 0.8 per cent of sodium chloride and 0.5 per cent of carbolic 
acid) should be at hand. Each of the small, colored bottles is to be 
filled with 9 ce of the diluent and marked with numbers, I, I, III, 
IV, V, VI, ete., respectively. Now take 1 ce of tuberculin and drop 
it into bottle No, I and shake it well, It now contains a 10 per cent 


UTILITY OF TUBERCULIN TREATMENT 767 


solution of tuberculin, so that a syringeful, with a capacity of 1 ce, 
contains 0.1 ce of tuberculin, or 100 ¢.mm. 

When we take 1 ce from bottle No. I and drop it into bottle No. 
II, we get a solution containing 1 per cent of tuberculin; one syringe- 
ful contains 10 c.mm. of tuberculin. Repeating the process, dropping 
1 ce from bottle No. II into bottle No. III, the latter will contain 
a 1 to 1000 dilution; 1 ce equals 1 ¢c.mm. of tuberculin; bottle No. 
IV, a 1 to 10,000 dilution; bottle No. V, a 1 to 100,000 dilution; and 
bottle No. VI, a 1 to 1,000,000 dilution, so that a syringeful will contain 
a dose of 0.001 c.mm. of tuberculin. These dilutions may be carried 
further and the dose, which should always be small, if administered at 
all, may be infinitesimally so. 

If given for its psychic effects, which is in fact done at present by 
most who use this agent, it is advisable to have ten bottles and that 
the first injection should be made from bottle No. X. If the patient 
is unpressed by the treatment, he will “react” at least with 0.3° 
to 0.5° F., which should satisfy anyone who is looking for a “mild 
reaction.” 

Moreover, there is no difficulty in administering properly a series 
of ascending doses of tuberculin, and no higher mathematics is neces- 
sary for its successful accomplishment. ‘Taking the first injection as 
a unit, we may increase the next injection by one-fourth or one-half. 
Thus, supposing we have used at first the dilution in bottle No. X 
containing 0.0000001 c.mm. of tuberculin per cubic centimeter, we 
inject but one-third or one-half of the contents of the syringe. The 
reaction is not likely to be severe, and we may one or two days later 
increase it to one-half or two-thirds of the contents of the syringe. In 
this manner we may proceed until we reach bottle No. VI, when the 
injection of a syringeful will give a dose of 0.001 c.mm._ It is not advis- 
able to give larger doses if we want to make sure that the patient is 
not harmed. But if there is any reaction the injections should be 
stopped promptly. 

Utility of Tuberculin Treatment.—It cannot, however, be denied 
that some good results have been obtained with tuberculin treatment. 
Whether they could not be obtained with other methods in those 
cases is another question. Thus, E. Rist! says: “For my part, I have 
never seen a patient doing well under tuberculin without remaining 
in doubt whether he would not have done as well without tuberculin. 
Nor have I met with cases where the influence of tuberculin was so 
strikingly favorable that I could feel justified in letting them abandon 
the classical treatment and rely on tuberculin alone.” Sir James Kk. 
Fowler says: “The tuberculin did not favorably influence the course 
of the disease in the majority of cases; in some cases the effects were 
detrimental; and even in stationary and improved cases it was difficult 
to ascribe any distinct improvement to the injections which might not 
have been equally attained under the treatment ordinarily employed 


1 Paris médical, 1913, 4, 241, 


768 SPECIFIC TREATMENT 


in the Brompton Hospital.” Likewise, Bardswell and Thompson,! 
in a recent statistical study of the experiences at Midhurst say that 
“collectively, the results point to the conclusion that tuberculin treat- 
ment, when given in addition to the usual measures practised in the 
sanatorium, had no appreciable effect either for good or ill. 
Unquestionably many patients who received tuberculin treatment 
made good recoveries, but there are no grounds for supposing that they 
would not have progressed as satisfactorily had the injections been 
withheld: certainly, comparable cases treated without tuberculin gave 
no less favorable results.” 

In the extensive Handbook on Tuberculosis, A. Schrider? shows 
that “it has been established that in institutions for the treatment 
of tuberculosis in which only general treatment is applied, the lasting 
results obtained are not inferior to those reported from institutions 
in which, in addition to the general treatment, so-called specifics are 
administered.” 

Good results are obtained with tuberculin only when carefully admin- 
istered in sanatoriums, with cases in the incipient stage, with but 
slight lesions, most of which are spontaneously curable. Although, 
according to Brown, at the Adirondack Cottage Sanatorium, no 
selection is exercised—the patients are allowed to elect tuberculin 
treatment. In private practice, as well as in most tuberculosis 
clinics in cities in this country, attempts with tuberculin have failed, 
evidently because the good surroundings, the fresh air, the proper 
food, regulation of rest and exercise were of more importance than 
the tuberculin. When we consider further that even the most ardent 
advocates of tuberculin state that only cases without fever, pursuing 
a slow course, showing no tendency to progress, but manifesting a 
strong tendency to fibrosis, are suitable for the treatment, it is clear 
that tuberculin is a remedy for those forms of phthisis which are 
spontaneously curable. 

Psychic Effects.—We have seen that the tuberculous patient is 
very amenable to suggestion (see p. 294) and we have pointed out 
that in a certain class of cases tuberculin produces excellent results 
for this reason. On this point a large number of physicians agree, and 
they continue to administer tuberculin because of its psychic effects, 
although they may as well administer distilled water hypodermically 
and obtain the same results. To keep nervous, irritable, fretful 
patients for months, or even for years, is a difficult matter; often it is 
an impossible affair. Something must be done in addition to the 
rest, fresh air, milk, and eggs, of which he believes he knows as much 
as his doctor. Such patients, when given tuberculin, told to watch 
out for reactions, to record in detail the symptoms produced by each 
ascending or descending dose on a specially prepared blank, are often 
very much encouraged. 


1 Pulmonary Tuberculosis, Mortality After Sanatorium Treatment, Med. Research 
Com., Special Report Series, No. 33, London, 1919. 
2 Brauer, Schréder and Blumenfeld’s Handbuch der Tuberkulose, 1915, 2, 3. 


a 


PSYCHIC EFFECTS 769 


This view of the psychic action of tuberculin is entertained by most 
authoritative physicians who use this agent extensively. Thus, Law- 
rason Brown,! who has done so much to popularize tuberculin in 
this country, says that only poor results can be expected when it is 
given “in cold blood.” He believes “its value can be greatly enhanced 
when the administrator has implicit faith in its curative properties 
and imparts that faith to his patients.’”’ Another significant reason 
for using tuberculin treatment, according to Brown, “is the closer 
relationship that such treatment establishes between patient and 
physician. I must confess that I find it difficult to bring a patient 
to my office twice a week for months and discuss symptoms and 
fears, one of which gradually grows less while the other is often replaced 
by more or less indifference, born of familiarity. When, however, 
I give this patient tuberculin, he and I can discuss his case in detail 
twice a week and I am able to discover slight but important changes 
in his condition, to check imprudence, and to change needless timidity 
into confidence in his ability to order aright his life.” 

But similar results have been obtained by Mathieu and Dobrovici 
with “antiphymose,” as was already detailed (see p. 657). In valvular 
heart disease, syphilis, myxedema, etc., this does not work. 

I believe that I am safe in saying that, as a rule, tuberculin treatment 
is only efficacious in intelligent patients who are under the impression 
that they have mastered the theoretical aspects of infection and 
immunity and of specific therapy from reading popular books and 
articles on tuberculosis. In fact, in my experience, uneducated patients 
hardly ever improve under tuberculin treatment because they cannot 
understand the benefit of fever, malaise, pain in the limbs, nausea, 
debility, ete. On the other hand, intelligent patients look forward to 
the reaction as an indication that the tuberculin is “working on their 
system” and they often improve, provided infinitesimally small doses 
have been given. 

There is no agreement among authorities as to what constitutes a 
“reaction” during tuberculin treatment. ‘All physicians are agreed 
that severe reactions are harmful to the patient, as a general rule,” 
say Archer W. R. Cochrane and Cuthbert A. Sprawson,? “but there 
is still considerable difference of opinion between those who like their 
cases to progress without any reactions at all, and those who prefer 
mild reactions as a routine. Again, opinion varies as to what con- 
stitutes a mild reaction. In dealing with those otherwise running a 
normal temperature, the limit by some has been fixed at 100.4° F., 
and reactions thereto are disregarded; that is to say, these physicians 
will increase the next dose if the dose has not given a reaction over 
100.4° F.”. But these authors consider this limit too high or dangerous, 
and are satisfied with a rise to 99.2° F. and call it a reaction. In 
other words, “the timid, or no-reaction school,” treat only afebrile 

1 Am. Jour. Med. Sci., 1912, 144, 524. 


» A Guide to the Use of Tuberculin, London, 1915, p. 60. 
49 


770 SPECIFIC TREATMENT 


cases. They should meet with immense success, because this class 
of patients recover spontaneously, or with any kind of treatment. 

Dangers of Tuberculin Treatment.—Since the first use of tuberculin 
as a therapeutic agent, it has been recognized that it is capable of 
doing irreparable damage when imprudently administered. Virchow 
found that it produced rapid disintegration of the tuberculous tissues 
in the lungs, caseous pneumonia, and at times eruption of miliary 
tubercles. More recent investigations have shown that it often mobil- 
izes the bacilli and thus may favor metastatic auto-infection. In fact, 
if phthisis was not a manifestation of immunity, disastrous results 
from this cause would be very frequent. It has also been observed 
that patients taking tuberculin for a long time are likely to develop 
nephritis. To be sure, with infinitesimally small doses the likelihood 
of such complications is reduced to a minimum, but the most experi- 
enced administrator is often surprised by unexpected reactions. I 
have seen such results repeatedly; mostly when tuberculin was admin- 
istered by such as were not skilled in handling this potent agent, 
but also at times in patients who were treated by very skilful physicians. 

Producing hyperemia of the affected lung area, tuberculin at times 
is effective in inducing pulmonary hemorrhage. When large doses 
were used this was very frequently observed and reported by Friinkel, 
Rumpf, Stricker, and many others. “Since small doses have been 
used,” says J. Sorgo,! “with a view of avoiding strong reactions, 
hemoptysis is only rarely observed after the administration of tuber- 
culin. At times small hemoptyses are seen, especially streaky sputum, 
but copious hemorrhages are rare. For this reason it is agreed that a 
tendency to hemoptysis is not altogether a contraindication to tuber- 
culin treatment, provided strong reactions are avoided.” But, as 
we already mentioned, this is not possible in every case. All who 
administer tuberculin for therapeutic purposes stop the treatment 
as soon as bleeding makes its appearance. 

The general practitioner should not use tuberculin at all. He can 
obtain the same results by the judicious use of drugs without incurring 
any risk. Even psychotherapy of the kind applied by those who 
administer tuberculin can easily be practised with medication, as 
was shown in Chapter XX XIII. 

Passive Immunization.—Active immunization through tuberculin 
having failed therapeutically, attempts have been made by many 
authors, notably Koch, Behring, Marmorek, Maragliano, and others, 
to cure the disease by passive immunization, or serotherapy. But the 
results have not been encouraging. It appears that so far we have not 
been able to raise the immunity to tuberculosis in animals to a degree 
that it may be transferred with the serum. Perhaps the reason is that, 
as far as our present knowledge goes, tuberculous immunity is hardly, 
if at all, humoral; in fact, it has been considered cellular by nearly all 
who have studied the subject. 


1 Brauer, Schréder and Blumenfeld’s Handbuch der Tuberkulose, 1914, 2, 255, 


CHA PTERGX LITE 
SYMPTOMATIC TREATMENT. 


Cough.—'To many patients the cough is the disease and they are 
under the impression that all they need for a speedy recovery is to be 
rid of this annoying and painful symptom. In its treatment some 
points are to be borne in mind: In most cases cough is decidedly con- 
servative—a purposeful reflex act; it removes the secretions from the 
respiratory passages which, if retained, might act like foreign bodies 
or produce toxic effects. But, on the other hand, cough often disturbs 
the affected tissues which need rest, if cicatrization is to occur, or it 
may be responsible for insomnia, hemoptysis, pneumothorax, ete. 
Bearing in mind the importance of rest in the treatment of this disease, 
it is clear that a coughing patient is not at perfect rest, but hard at work. 
At times the reduction in the fever which absolute rest brings about, 
is obviated by the cough. Usually these conflicting principles can be 
reconciled by appropriate treatment. 

Cough can be prevented or ameliorated by simple measures in a 
large proportion of cases. Atmospheric purity contributes consider- 
ably toward a reduction in its frequency and severity. Outdoor 
life and good ventilation of the room inhabited by the patient meet 
this indication. Mouth-breathing is a cause of excessive coughing in 
many cases, and some get fits of coughing when suddenly changing 
from a warm into a cold atmosphere, or the reverse. In steam-heated 
rooms, in which the air is usually dry, cough is more frequent than in 
rooms in which the air contains a proper amount of moisture. 

In advanced cases with secreting cavities, the cough may be influ- 
enced by posture; reclining on one side, expectoration is facilitated, 
while lying on the other side brings about violent fits of coughing. 
Patients soon find out which position gives them relief and recline 
accordingly. However, it is best for some patients to recline on the 
side which induces cough and thus clears the chest securing rest in the 
interval. Many patients cough only during the morning hours and 
thus empty the cavities of the secretions which have accumulated dur- 
ing the night, while during the day there is but little cough. They 
need no treatment for this symptom. 

It will be observed that some phthisical patients who sleep well 
during the night, cough more during the day than those who cough 
more or less during the night. The administration of large doses of 
opiates during the evening may gain relief in sleep, but also result in 
miserable hours during the following day. This is to be remembered 
when administering opiates to tuberculous patients, 


re SYMPTOMATIC TREATMENT 


Psychotherapy of Cough.—It is a noteworthy fact that the cough is 
greatly influenced by the psychic state of the patient. Persons with 
an irritable nervous system, the hysterical, emotional, and neurasthenic 
cough more than the dull, the phlegmatic and apathetic. Some cough 
while in the house, and are relieved as soon as they go out into the 
open air, while in others the cough increases as soon as the window is 
opened, or when they go out into the open air on a cold day. This 
last class of patients is very difficult to manage. 

Other psychic influences are seen in patients who usually cough 
excessively, but cease when in agreeable company, or are intensely 
interested in something, ete. I have practically stopped unproductive 
cough in many patients by threatening them with expulsion from 
the hospital if they did not cease annoying their fellow-sufferers in 
the ward. Lonesomeness, and also insomnia are often responsible 
for excessive cough and should be treated according to indications. 
In sanatoriums the influence of example is often very good: ‘The 
patient sees others control their cough and attempts to do likewise, 
and is often surprised at his success. 

The patients can, within certain limits, control their cough, as 
Galen pointed out more than seventeen centuries ago, and Dettweiler 
has shown that this symptom can be “disciplined.” Even when 
the cough is productive of considerable quantities of sputum, the 
patient is to be instructed that he need not expel it all at once; that 
if he succeeds in suppressing it for some time, the accumulated sputum 
will later be brought out with little effort. During the morning 
hours patients often make strong efforts to clear their chests. But if 
they wait till after breakfast they find in many cases that the sputum 
comes up easily. ‘Cough induces cough,” says Penzoldt,! and for 
this reason patients are to be warned against giving in to the first 
tickling of the throat. The great struggle will only be during the 
first two or three days. Meeting with success, patients become con- 
vinced of their own powers to suppress, or control this symptom. 

But patients must be warned in this connection against swallowing 
their sputum—“ spitting into their own stomachs.” Controlling does 
not mean entirely suppressing expectoration, as women and some 
men are apt to do. The dangers of the habit are to be explained in 
detail to the patient. 

I cannot agree with those who prohibit smoking to tuberculous 
patients indiscriminately. To be sure, those who are not accustomed 
to tobacco often cough when near a person who smokes. But many 
habitual smokers are greatly relieved by a cigar or a cigarette. Our 
advice should be in accordance with the experience of the individual 
patient. 

Many home remedies are very often efficacious in relieving cough. 
Thus, equal parts of boiled milk and honey or glycerin, with or with- 


1 Handbuch der Therapie, 1910, 3, 249. 


COUGH 173 


out a flavoring agent, may be of great use in stopping an annoying 
cough. An aha remedy is the application of a small mustard 
leaf or blister over the seat of the lesion. It may be repeated from 
time to time. The fact that it works by psychic suggestion should not 
deter us from using it, so long as the patient gets relief. 

Medicinal Treatment.— After all the cases in which the cough may 
be controlled, or made bearable, by simple methods are ieee iitedls 
there remains a large number who must be given sedatives to control 
this symptom. In the incipient stage these remedies are only rarely 
called for, and then only for a short time. But in advanced cases the 
indications for sedatives become more and more urgent. As Penzoldt 
says, the more progressive the disease and the less the chances of 
ultimate recovery, the more the charity of morphine is to be dispensed 
to the unfortunate sufferer. 

In my experience, many cases in the incipient and moderately 
advanced stages of the disease are immensely relieved by creosote and 
its derivatives. The method of administration is given elsewhere. 
In those in whom internal administration does not relieve the cough, 
we may try the effects of inhalation of creosote, menthol, eucalyptol, 
tincture of benzoin, etc. The following is as good as any that has | 
been recommended: 


R—Creosoti, 

Acidi carbolici, 

Spt. chloroformi . . Me aos a 1Vs 15.0 
M.S.—Ten to twenty droped in an AES to be used for fifteen minutes at a time. 


Failing with these simple remedies we must resort to anodynes in 
case the cough is frequent, violent, paroxysmal, or disturbs the patient’s 
comfort or sleep. Of these, cannabis indice is the least harmful and 
should be given the first trial. The extract may be given in doses of 
+ grain in pill or tablet form several times a day. In spasmodic cough 
it may be combined with hyoscyamus or gelsemium. The following 
may be used to great advantage: 


R—Extracti cannabis indice 5. 6, A LS, Se Fee 0.4 
iixtractiohyOscyamiuw. ss p20 ieee eli 6 SPT. Xi 0.8 

M. ft. pil. No. xxiv. 

S.—One pill four to six times a day. 


R—Extracti cannabis indice fl., 


Extracti gelsemii Seer enh Se ee PRS Ty 8.0 
Syr. acacize : oe Pe a hie ee oe eS See a 30.0 
Aquze menthze piper. : #6 A Evel date 120.0 


M. 8.—One teaspoonful four times a aay. 


In many cases nothing but opiates gives relief. But in incipient cases 
opium and its derivatives are to be avoided because they may have to 
be continued for long periods and, in hopeful cases, the danger of habit 
formation is not negligible. In addition, opium deranges the digestive 
functions, produces anorexia and constipation, slows the frequency 


774 SYMPTOMATIC TREATMENT 


and the amplitude of the respiratory movements, and favors stag- 
nation of the secretions in the respiratory passages. A dose of Dover's 
powder may be given in the evening now and then with a view of 
controlling the cough during the night, but to continue the adminis- 
tration of opium in any form for any length of time is dangerous. 

Of the many opiates, codein, which is ten to twelve times less toxic 
than morphine, is to be preferred. It may be given in tablet form in 
doses of + to + grain, and in advanced cases in much larger doses 
several times a day; or it may be added to any other medication that 
is being administered. Thus I quite often add it to creosote medica- 
tion: : 


R—Gualscolis carbonatis!ai) bee aL enn a) Beene LISS 10.0 
purychnins sulphatisseeew eee eer Ty 0.06 
ATSCRICL Crio Idi \oeuee nin Geen ae ee CTR) 0.06 
Codeinssphosphaticums a) le ane Ig 0.5 

M. ft. capsul. No. 50. 

S.—One capsule three times a day after meals. 

R—Codeine sulphatis A is Nee os LT) he Se OT 0.3 
Extracti cannabis indice Je Ame ye eects 0.4 
Eixtracty: belladonns 5) sp ee net OT aT) 0.2 
extract, elycyrtbizce et eee ee ee ee OT oT 0.8 


M. ft. pilulee No. xii. 
S.—One pill at night. 


In most cases in which sedatives must be given for a considerable 
time the dose must soon be increased because after a few weeks the 
effects on the cough are diminished. Instead of increasing the dose, 
we may do better by changing one for some other derivative of opium. 
Heroin may be given in doses of 54; to } grain according to indications. 
It does not constipate and when there is dyspnea it is the best palliative 
remedy. It is to be regretted that because of its habit-forming 
potentialities, some hesitate in using it, and strong efforts have of late 
been made to discourage its use in practice. I have had no cause to 
regret prescribing it for these reasons, though I have used it in daily 
practice for many years. In incipient or favorable cases the chances 
of inducing a habit are remote; I have not met with a case. In far 
advanced and hopeless cases there is no harm done. Why not make 
the last earthly days comfortable? Dionin is another of these prepara- 
tions and, when insomnia is a troublesome feature, it is even better 
than the above. Not many cases of habituation to dionin have been 
reported, but it is more apt to cause constipation than codein or heroin. 
The two last-mentioned preparations do not interfere with the expec- 
toration of sputum; some even maintain that they assist in its expulsion. 
Whenever feasible, these narcotics are not to be given after midnight in 
order to avoid headache and debility durmg the morning hours. 

The emetic cough is a very difficult symptom to control in some 
cases. I have seen some in whom it was responsible for a bad turn in 
an otherwise favorable case. Rarely, no food can be retained. In 


EXPECTORATION 775 


many cases it may be relieved by avoiding heavy meals—taking several 
small meals during the day. The patient should recline in bed immedi- 
ately after meals and avoid any exertion, and even speaking. But at 
times we must resort to medication. Some have reported good results 
from several drops of chloroform well diluted, or from bromoform. I 
have had cases in which only cocain administered before meals was 
effective in retaining nourishment in the stomach. The following 
prescription of Albert Robin may have to be resorted to: 


R—Coeain hydrochloratis es i A, oR ree [Ono Soret 0.06 
C@ocdeinarcul pha tse on a ner er | 0.06 
IAGUseTeRlOrOlLOLMal se oe ne) oly 60.0 
ANOLE oo | A Ba, Pade Siv 120.0 


M. 8.—Tablespoonful after meals. 


Expectoration.—In the average case of phthisis expectoration is a 
salutary phenomenon, removing, as it does, foreign, often toxic, 
material from the respiratory passages. At times it becomes excessive 
and annoying, but it should never be suppressed. In some cases with 
extensive excavations the amount of sputum brought up may be 
controlled within limits by posture. We advise our patients to recline 
in certain positions which favor the expulsion of sputum and thus 
empty the cavities of their contents. Relief may thus be obtained 
for the rest of the day. In cases in which the sputum is fetid—rare 
in phthisis—antiseptic inhalations may be tried. Creosote, iodine, 
menthol, eucalyptol, turpentine, etc., may be inhaled through an 
inhaler or simply dropped in hot water and inhaled. 

Very often patients complain that they feel heavy on the chest and 
that if they could only brmg up sputum they are confident that they 
would be relieved. Many drugs have been used for this purpose, 
especially the so-called expectorant remedies. It seems that all that 
is usually attained is a disordered stomach. 

It appears from recent pharmacological investigation that there are 
no drugs which, when given in small doses, will induce more abundant 
secretion into the respiratory passages, stimulate the cilia of the 
bronchial mucous membrane to bring out secretions, or render tena- 
cious secretions more easily movable from the bronchial walls to which 
they adhere. J. L. Miller! found that ammonium carbonate and 
ammonium chloride, and the emetic group of expectorants, as apo- 
morphine and ipecac, when given in sufficiently large doses to animals, 
increase the bronchial secretion. Ammonia salts per os, in moderate 
doses equivalent to 2 mg. in an adult man, do not increase bronchial 
secretions in the dog. Apomorphine and emetin, when given to dogs 
in doses considerably greater than the ordinary therapeutic dose for 
man, do not excite increased bronchial secretion. 

It is therefore absurd to give nauseating potions of ammonium salts, 
senega, ipecac, apomorphine, etc. All we may succeed in doing is to 


1 Am. Jour. Med. Sci., 1914, 118, 469. 


776 SYMPTOMATIC TREATMENT 


disorder the stomach, but the secretion in the respiratory passages 
remains unaffected. 

In fibroid phthisis it has been found empirically that potassium 
iodide, or iodides in other forms, facilitate, expectoration and give 
immense relief to suffering patients. The same is true of other chronic 
afebrile cases of pulmonary tuberculosis. I have been using iodides 
in this class of cases with benefit for many years. 

Fever.— ever is an indication of active, often progressive phthisis, 
unless due to some complication. Its continued presence proves con- 
clusively that the disease is spreading, even if the physical signs remain 
unaltered. It is at times neglected or overlooked because, unlike fever 
in other diseases, the patient in spite of a temperature of over 100° F. 
may feel quite comfortable, have a good appetite, and even gain in 
weight. But the entire future of the patient may depend on the 
treatment of the fever; neglecting mild febrile attacks means an invita- 
tion for chronic prolonged fever with lessened chances of recovery. 

During the initial stages of the disease fever demands rest in bed, 
not so much as a cure but as a preventive against the extension of 
the process in the lung. It is remarkable that in many cases the fever 
abates within a few days or a week only through an improvement in 
the hygienic conditions and the diet of the patient, and placing him 
in a light and well-ventilated room. It is unfortunate that very few 
patients are willing to submit to perfect rest at this stage, claiming 
that they are not sick. 

There are many advanced cases of phthisis with quite extensive 
lesions in which there is a daily rise in the temperature of 1 to 1.5° F., 
but the patients feel quite well and are even able to pursue their 
vocations. ‘They need no active treatment because they have become 
habituated to the subfebrile temperature which may be regarded as 
their normal condition. In them the tubercle bacilli have actually 
become saprophytic and give them no trouble. In this class of cases 
it is only necessary to take steps to reduce the temperature when the 
patient is clearly suffering as a result of it; when the fever produces 
symptoms such as anorexia, restlessness, irritability, insomnia, etc.; 
or when he is losing in weight. I have observed many cases in which 
fever was due to overfeeding, and a reduction in the quantity of food 
promptly brought the temperature down to normal. 

A sudden rise in the temperature in the course of chronic phthisis 
may be due either to an extension of the lesion, a new pneumonic pro- 
cess in a hitherto unaffected part of the lung, or to some complication. 
The former demands rest in bed till the temperature comes down to 
normal; in the latter the indications are in accordance with the patho- 
logical conditions which present themselves. 

Patients are apt to attribute an attack of fever to “indigestion,” 
but im my experience acute gastritis is a rather infrequent cause of 
pyrexia in phthisis, though a dose of calomel at times relieves an 
evanescent febrile attack. But then we‘may suspect that the relation 


FEVER Ge 


was merely coincidental, a frequent source of error in therapeutics. 
More often fever lasting several days is due to some intercurrent mild 
or severe infection. In hospital practice there is seen at times an 
actual epidemic of obscure infections; most of the patients in a ward 
are attacked during a period of a couple of weeks. The treatment is 
rest in bed and some antipyretic, like antipyrin, quinine, aspirin, etc. 
Complicating pleurisy, with or without effusion, may be the cause of 
a rise in temperature. In some women premenstrual, or menstrual, 
fever demands rest in bed periodically for a few days. The instability 
of the temperature in phthisis, which has been discussed in a previous 
chapter, is responsible for many febrile attacks. Any physical or 
mental exertion, worry, grief and anxiety may raise the temperature 
several degrees. Prophylactic and curative action is indicated along 
these lines. In many patients who have become “thermometer 
fiends,” getting excited after reading the thermometer, it is best to 
prohibit the using of this instrument of precision, and to keep the 
fever chart away from them. Very often improvement takes place 
soon after these simple measures are taken. 

The fever accompanying active phthisis demands active treatment. 
The main aim should be to remove it, or to prevent its occurrence. If 
we fail in this, we fail in our efforts at relieving the patient. It may 
very often be prevented by putting a patient to bed at the very first 
indication of a tendency to hyperthermia from any cause. Indeed, 
the neglect of mild febrile attacks is very often responsible for prolonged 
and even fatal fever. 

In high continuous fever perfect rest is indicated, preferably in the 
open air, or in a room with wide-open windows, as has already been 
detailed in Chapter XX XVII. The patient is to be treated as though 
he is suffering from an acute disease, like typhoid or pneumonia. It is 
often surprising to note the prompt improvement after a rest in bed 
for afew days. Patients with a temperature at a high level for several 
months are often difficult to manage. When accompanied, as it 
usually is, by progressive loss of appetite, weight, and strength, they 
become discouraged and rebel against the prolonged and strict con- 
finement. In such cases, provided the temperature is below 101° F., 
the experiment may be made of permitting them to leave the bed and 
get out in the open, resting on a reclining chair for a few hours during 
the day. The best hours are before or around midday, when the tem- 
perature is usually at its lowest; but any other time may be chosen 
under the guidance of the thermometer. In hectic cases the tempera- 
ture is usually at its lowest in the morning and the patient may be 
allowed to leave his bed at that time. I have seen many patients, who 
did badly for weeks, improve when allowed to remain in the upright or 
semi-upright position for several hours a day. But care and circum- 
spection are to be exercised while applying this treatment. 

Some patients may be sent to the country and the change is at times 
effective in reducing the temperature when everything else has failed. 


778 SYMPTOMATIC TREATMENT 


But this is not available to patients who have not the means to leave, 
accompanied by an attendant. Many authorities state that a moun- 
taimous climate is to be preferred for this purpose, but in my experience 
any change may do just as well. 

It is deplorable that public sanatoriums do not admit febrile cases. 
Great service could be rendered by removing the patient for several 
weeks, during the period of fever, to better surroundings, giving him 
an opportunity to rest without interference by well-meaning, but often 
ill-guided, relatives and friends. I have often felt that cases under 
my care could be saved if sanatoriums were managed along hospital 
lines, admitting patients during acute exacerbations in the places 
which are now filled with patients whose condition is such that they 
would do well in any healthy surroundings which can be obtained in 
the average home. 

When the temperature is not much above 100° F., the diet of the 
patient need not be different from that given in the usual case of active 
tuberculosis. Patients running higher temperature should not be 
starved. A rich, but easily digestible diet is indicated. Because of 
the anorexia, and actual distaste for food which these patients mani- 
fest, as a rule, the food must be appetizingly prepared, and here again 
a good cook can do a great deal. In many cases, to avoid cachexia in 
prolonged fever, some of the stomachic bitters should be administered 
with a view of improving the appetite. Whenever possible, milk 
should be used as a beverage in addition to the usual food, and given 
between meals. Some patients need alcoholic beverages and they 
should get them, because at times they are the best agent to improve the 
appetite and promote digestion. Patients with hectic fever are often 
benefited by some whisky an hour before the expected chill. 

Hydrotherapeutic measures have not been found satisfactory in the 
treatment of fever in phthisis. The use of ice, or of cold sponging, or 
bathing, although possibly of temporary benefit, is contraindicated 
in most cases because they are apt to depress the patient. The most 
that can be done is to give a warm or tepid bath once or twice a week 
for the purpose of cleansing the body, but care is to be taken not to 
subject him to overexertion while going and coming from the tub. 
The fact that hydrotherapeutic methods have been given up in nearly 
all sanatoriums is sufficient proof that they have not been beneficial; 
in fact, that they are harmful. 

Artificial pneumothorax is an excellent radical measure against 
tuberculous fever in appropriate cases. This will be discussed in 
Chapter XLV. 

Antipyretic Medication.— Antipyretic drugs should only exceptionally 
be used in phthisis. In the first place, tuberculous patients do not, as 
a rule, suffer from the pyrexia to the same extent as patients with 
typhoid fever, pneumonia, etc., and a reduction in the temperature 
does not necessarily give the relief which the patient anticipates. It 
is not the fever, excepting hyperpyrexia, which is dangerous, but the 


NIGHTSWEATS 779 


activity of the tuberculous process, and so long as only the former is 
influenced, the patient is not materially benefited. 

The action of antipyretic drugs is ephemeral and deceptive, often 
accompanied by profuse perspiration which is enervating; and by 
digestive disturbances. Large and frequently repeated doses are 
necessary for weeks in the usual case and their action on the heart, 
which is not salutary, often leads to collapse. 

But when the fever is high and continuous, or accompanied by head- 
ache, backache, and debility, one of the coal-tar antipyretics may give 
comfort with or without reducing the temperature. Acetanilid is to 
be avoided for well-known reasons. Phenacetin acts too quickly and 
produces profuse sweating. Antipyrin, or better pyramidon, may be 
used in 5- to 10-grain doses, combined with caffeine. Patients may 
stand the fever without complaining much, but in septic cases they 
abhor the chills which are apt to occur before the onset of the pyrexia. 
The best treatment is to place the patient in bed a few hours before the 
appearance of the chill, cover him well, and given him a drink of hot 
lemonade, tea, or whisky and, in severe cases, a dose of pyramidon. 
The chill may not be prevented completely in this manner, but it is 
rendered bearable. On the whole, antipyretic medication is to be 
administered an hour or so before the highest temperature is expected, 
varying with each case. Quinine should be given, if at all, five to six 
hours before the maximum temperature is expected, while pyramidon, 
antipyrin, aspirin, etc., require but two or three hours. When the fever 
has declined medication should not be continued, otherwise collapse 
may occur. 

The salicylates are often very good in these cases, especially in the 
chronic hectic fever of consumption. The old prescription of sodium 
salicylate and arsenous acid (sod. salicyl., 10; acid. arsenicosi, 0.01; 
ft. pil. no. 100; S., five to ten pills three times a day after meals) is 
very good. But I have found that 7 to 10 grains of aspirin and ;4> 
gr. of arsenic in capsule three times a day are better. It is less likely 
to disturb digestion. But in patients showing a tendency to hemop- 
tysis the salicylates are to be avoided. Pyramidon is best for this 
class of patients. 

An excellent remedy for fever in tuberculosis is guaiacol painted with 
a camel-hair brush on the skin in 7- to 15-drop doses and covered 
air-tight. The temperature drops sometimes within one hour. It is 
best to rub into the skin of the thorax a teaspoonful of a 10 per cent 
guaiacol-vaseline ointment two or three times a day. It must be 
mentioned that collapse has been observed in some cases after the 
application of guaiacol. 

Nightsweats.—No other symptom of chronic phthisis is more dis- 
couraging and enervating than nightsweats and their relief is of 
immense importance. It seems that in the vast majority of cases they 
can be prevented without the use of medication, and many physicians 
state that with careful prophylaxis they have not used any drugs for 
this symptom for years. 


780 SYMPTOMATIC TREATMENT 


Open-air treatment is the best preventive of nightsweats. Sleep- 
ing in a cool room with sufficient, but not excessive, coverings must 
be enjoined. It is also good to give the patient before retiring a glass 
of cold milk with three or four teaspoonfuls of cognac to prevent the 
rapid sinking of the pulse-rate. In some cases a roll with butter may 
serve the same purpose. Some patients may be relieved by noting the 
time of the beginning of the sweating, and waking them a few minutes 
before and giving them an ounce of whisky. For private patients an 
alarm clock may be used for the purpose. This method, recom- 
mended by William Porter,! should be tried in all obstinate cases. 

In cases in which these simple measures do not succeed, the sulphate 
of atropin in doses of ;+y grain, given in tablet form about seven 
o’clock in the evening, may give complete relief. Agaricin is also good 
in doses of 5'5 grain, but it acts more slowly and must be administered 
about six hours before the sweating is expected. It often produces 
gastro-intestinal disturbances, especially diarrhea, and should be com- 
bined with an opiate—Dover’s powder in 3- to 5-grain doses. Cam- 
phoric acid, in 10- to 20-grain doses, may be tried in obstinate cases. 
It is to be remembered that no remedy retains its power over this 
symptom for a long time, and after one ceases to act, we may try 
another. 

Friction of the skin with tepid water, vinegar, or alcohol and water, 
or a 3 per cent lysol solution, may give relief. 

Hemoptysis.—The prophylaxis of hemoptysis cannot be considered 
a simple matter despite the fact that we speak so much about the pre- 
disposing and exciting factors of pulmonary hemorrhage. Patients 
with really initial hemorrhages nearly always consult us only after the 
accident has occurred. Overexertion, excitement, etc., as exciting 
causes of pulmonary hemorrhages, have recently been shown to have no 
etiological relation in the vast majority of cases. It appears that most 
hemorrhages, especially those which are copious and fatal, occur during 
the night, or when the patient has been at rest. 5S. Bang? has recently 
made a special study of this problem and found that among 2000 tuber- 
culous patients in a sanatorium, the initial hemorrhages came on while 
the patients were lying in bed, or on a reclining chair, in 69 per cent of 
354 cases; in 15 per cent while they were dressing, sitting up in bed 
or just lying down; and in only 6 per cent of cases while the patients 
were walking or working; and in 8 per cent while they were otherwise 
engaged. In only 2 of the total number were the patients climbing 
stairs, though he estimates that these 2000 patients must have climbed 
the stairs over a million times, and taken 10,000 warm baths, and 25,000 
douches while at the sanatorium. These facts, which may be dupli- 
cated by observations of any physician with large experience, show 
conclusively that overexertion is but a negligible factor, if any at all, 
in hemoptysis. 


1 International Clinics, Sixteenth Series, 1906, 4, 77. 
2 Ugeskrift for Laeger, 1916, 78, 419. 


HEMOPTYSIS 781 


It appears that in active and progressive cases pulmonary hemor- 
rhage is often the accompaniment of acute exacerbations of the disease. 
In rare cases we meet with hemoptysis, or even with fatal hemorrhages, 
in an entirely afebrile patient. But in most instances, fever, tachy- 
cardia, etc., precede the onset of the bleeding by several days. Bang’s 
statistics substantiate this observation. Many patients suffering 
from acute exacerbations, or from febrile complications, have attacks 
of hemoptysis; at times, profuse hemorrhages. The prophylaxis in 
these cases is thus clearly the prevention of the acute exacerbations, 
or the febrile complications, which are liable to produce stasis and con- 
gestion of the involved lung area. The smaller hemorrhages are usually 
the result of diapedesis, being of parenchymatous origin, and have 
nothing to do with the position of the body, nor with overexertion or 
excitement. 

The copious pulmonary hemorrhages, due to erosion of a pulmonary 
bloodvessel, can hardly be foreseen nor prevented; they are due to 
the involvement of a bloodvessel in the tuberculous process, with 
softening of its wall, thus allowing the blood to escape before a thrombus 
has formed. In others, it is due to the rupture of an aneurysm of 
Rasmussen, as was already shown in the chapter on Pathology. To 
speak in these cases of prophylaxis is futile. 

All patients with pulmonary tuberculosis are to be told in advance 
that there is less danger in. blood-spitting than is generally believed. 
We would thus avoid the psychic depression which is so often an 
accompaniment of hemoptysis. Women may be told that in the aver- 
age case of hemoptysis there 1s no more danger than in the loss of blood 
during the menstrual period. 

Not all cases of hemoptysis require the same treatment; individuali- 
zation is required here, just as in most other pathological conditions. 
The vast majority of hemorrhages. are insignificant, and if we only 
quiet the patient by an assurance that there is little danger, the 
bleeding will cease sooner or later, and the underlying process in the 
lung pursues its course uninfluenced by the accident. This is true of 
streaky sputum, which often terrorizes a patient to the same extent as 
a copious hemorrhage. But when the blood brought up is bright red, 
even if only a few mouthfuls, the matter is to be taken more seriously, 
because these small hemorrhages are at times the precursors of repeated 
and copious, though rarely uncontrollable, hemorrhages. As a rule, 
the fatal hemorrhages are copious and uncontrollable from the very 
beginning. 

The patient is put to bed, but not in the traditional prone position. 
The blood and sputum must be evacuated from the respiratory pas- 
sages with ease, and this can only be done when the patient is in the 
semi-sitting position. In this manner nourishment and medication 
can be administered without unduly disturbing the patient, expectora- 
tion is facilitated, and in copious hemorrhages, atelectasis of the pos- 
terior parts of the lung is prevented; eating, the administration of 


782 SYMPTOMATIC TREATMENT 


medicines, vomiting, and the toilet, are thus facilitated. The time- 
honored ice-bag applied to the chest is of no value at all, excepting to 
keep the patient busy and attentive while attempting to keep it in place. 

I have thus treated during the past five years nearly all the cases of 
hemoptysis under my care and found that the bleeding ceased just as 
quickly as when I applied the rigid-rest treatment. The psychic effect 
has even been more salutary. The patients are not so frightened as 
when they are warned that the least motion of the body, any word 
uttered, may increase the bleeding. It is best to place the patient in 
the semi-upright position immediately after the bleeding begins, 
because, as has been pointed out by Bang, rising in bed from the recum- 
bent to the sitting position involves contraction of the abdominal 
muscles. These are liable to press upon the vena cava as in straining 
at stools, and by reflex action from the splanchnic nerve, cause an 
increase in the bleeding. This is probably responsible for the experi- 
ence that sitting up in bed causes an increase in the flow of blood. It 
may be averted by placing the patient from the start in the half-seated 
position. 

The therapeutic indications to be met are: Prevention of excessive 
cough and expectoration; increasing the coagulability of the blood 
and immobilization of the bleeding lung. 

Morphine. — To allay excitement, procure rest, and thus prevent exces- 
sive cough, there is no better remedy than a hypodermic injection of 
morphine. We must bear in mind that we are in the presence of a 
conflicting situation. On the one hand, we must see to it that the 
effused blood in the bronchial tree should be removed; on the other 
hand, the strong expiratory efforts necessary to accomplish the expul- 
sion of the blood and clots are accompanied by an increase in the 
pressure in the pulmonary circulation and, with their removal, the 
thrombi which plug the bleeding vessel are dislodged, and thus renewed 
bleeding is likely to occur. Morphine meets but one of these indica- 
tions: It depresses the cough center, diminishes the frequency and 
amplitude of the respiratory movements, and quiets the mental state 
of the patient. Some have even found that morphine increases the 
coagulability of the blood. But after all it has its dangers. When 
given to excess, as is often done, it depresses the respiratory center, 
paralyzes the sensibility of the bronchial mucous membrane, and thus 
interferes with the expulsion of the blood and clots. Aspiration 
pheumonia may thus result in cases in which it is more successful as 
a hemostatic than is desirable. 

For this reason morphine is to be used with great care and circum- 
spection. Tinding the patient excited and in agony, we inject hypo- 
dermically } grain of morphine for its general and local effects. If the 
bleeding does not stop within an hour, the morphine should not be 
repeated, but other means are to be taken to control the hemorrhage. 

Salt.—An ancient remedy for copious pulmonary hemorrhage is the 
administration of table salt. Formerly it was thought that because 


HEMOPTYSIS 783 


it acts as an emetic, and thus depresses the blood-pressure, it is of use 
in hemoptysis. But we now know that its modus operand is different. 
Von den Velden! has proved that, in man, swallowing 5 to 15 grams of 
table salt increases the coagulability of the blood within five minutes. 
Within one hour the coagulability returns to its former intensity. 
Sodium bromide has nearly the same effect. For this reason the 
administration of 5 to 10 grams of table salt, or 3 grams of sodium 
bromide, three or four times a day, may prove of immense value in 
hemoptysis. In very nervous patients the bromide is to be preferred. 

More recently salt has been administered intravenously in isotonic 
solution, as reeommended by Hans Miiller.2 Ten to 50 ce of a 10 per 
cent solution of sodium chloride, sterilized and heated to the body 
temperature, are injected into the median basilic vein, great care being 
taken not to drop any of the solution into the subcutaneous tissue, 
~ which is likely to cause intense pain. I have tried this treatment but 
have not found it superior to other methods. 

Tying the Extremities.—The coagulability of the blood is also in- 
creased by tying up the blood in the extremities. A constricting band, 
or a tourniquet, is tied around the arm and the hip; two or three of the 
extremities are tied up at a time. In order to avoid injury to the 
nerves a roller bandage, or any other soft pad, should be placed under 
the tourniquet over the path of the larger vessels. The bandage should 
not remain in place for more than two hours, otherwise muscular 
paralysis or necrosis of the skin may result. As a rule, one-half hour 
is sufficient. The bandage is to be loosened slowly, by degrees, for 
obvious reasons. 

Artificial Pneumothorax.—In cases in which the above measures are 
of no avail, the induction of an artificial pneumothorax may be con- 
sidered, provided it can be ascertained in which side of the chest the 
bleeding is going on. This point is discussed elsewhere in this book. 
But it should be stated that in very acute cases, in which the exsan- 
guination is sharp and brisk, there is usually nothing to lose and, even 
when we are not sure, we are justified in inducing a pneumothorax in 
the pleura of the lung which is most likely the source of the bleeding, 
as shown by clinical indications. When the bleeding lung is collapsed, 
the bleeding stops immediately. 

Medicinal Treatment.—It will be noted that we have left to the end 
the numerous drugs which have been used for the purpose of allaymg 
pulmonary hemorrhage. The reason is that we do not know of any 
drug which will stop hemorrhage in the lung. It seems to me that the 
reputation of some drugs as pulmonary hemostatics has been acquired 
on the basis of the fact that the vast majority of hemorrhages stop 
spontaneously; anything will do and receive the credit. This appears 
to be the consensus of opinion of phthisiotherapeutists at present, 


1 Ztschr. f. exper. Pathol. u. Therapie, 1910, 7, 290, 
2 Beitr. z. Klinik d. Tuberkulose, 1918, 28, 1, 


784 SYMPTOMATIC TREATMENT 


although no less an authority than Albert Robin' says that he 
feels constrained to protest vigorously against the allegation that 
medicinal agents are impotent, and are only given credit for their 
psychic effects. To be sure, he says, there are many cases of hemop- 
tysis which stop spontaneously, with or without treatment; there 
are others which cannot be controlled by any treatment. But between 
these two extreme types there are many cases in which medicinal 
treatment has a decidedly beneficial influence. 

Emetin.— In former times emetics were given in hemoptysis and excel- 
lent results were reported because, with the vomiting, the effused blood 
in the bronchi was also expelled, preventing asphyxiation and also 
because the nauseous feeling reduced the blood-pressure perceptibly. 
Following Trousseau’s suggestion, large doses of 1pecac were given for 
this purpose. But we now have in emetin an excellent substitute for 
the nauseous Ipecac. It acts as a hemostatic when many other agents 
have failed. I have used it in 3-grain doses, repeated three to five 
times a day, with satisfaction. The simplest way of administration in 
these cases is hypodermically. Either the tablets or the ampoules, 
which many pharmaceutical houses prepare, may be used for the 
purpose. It appears that emetin is useful in cases of hemorrhage 
when there is no fever. Patients with fever above 101° F. are hardly 
ever, if at all, benefited by this drug. 

The Nitrites.—The nitrites have been found efficient in checking 
the bleeding from the lung. They are known to lower the blood- 
pressure and this may be the cause of their efficacy. Macht? found 
experimentally that the nitrites cause a constriction of the pulmonary 
vessels and at the same time they are efficient peripheral and splanchnic 
vasodilators. As usually given in 2 or 3 drops, amyl nitrite is often 
inefficient. I found that J. E. Squire’s® suggestion to give 10 to 15 
drops, dropped on a handkerchief which is placed before the patient’s 
mouth and nose, is best. Immediately the face becomes red and con- 
gested and the hemorrhage stops. It may be repeated several times 
during the day. In more copious hemorrhages, where the nose becomes 
blocked up with blood and clots, it may be necessary to put from 30 
to 50 minims on a piece of lint and hold it over the patient’s mouth. 
It may have to be repeated and the only complaint heard from the 
patient is that it produces a feeling of nausea. C. Fochi* says that 
when administered as soon as the first traces of blood-spitting are 
seen, copious hemorrhages may be prevented. But this is open to 
question. Fatal hemoptysis only rarely begins with streaky sputum. 
It is copious from the start, as a rule. 

In slow bleeding, nitroglycerine, given in small and frequently 
repeated doses, as recommended by Flick, is often of service. When 


Thérapeutique uselle de la tuberculose, Paris, 1912, p. 294, 
Jour. Am. Med. Assn., 1914, 62, 524. 

Clinical Journal, 1909, 34, 155. 

Gazetta degli Ospedali, 1908, 29, 114. 


eo ow 


HEMOPTYSIS 785 


administered in 2- to 4-drop doses of the 1 per cent alcoholic solution 
it produces the same effect as amyl nitrite, but slower and more lasting 
effects are observed. Tablets are not to be trusted because they are 
often mert, as has been shown by George B. Wallace and A. I. Ringer.! 
The 1 per cent solution, as represented by the pharmacopeial spirits, is 
the best form in which glonoin should be administered. The following 
formula may be prescribed: 


R—Spirit. glonoini eet meee Cee Pee ol i) eoaoe tol 4.0 
ACIcoRAUIT ATC LINOT nee: | ure ae eG es sy 30.0 
Aque destil. . . See te ee Vi 120.0 


M. 8.—One teaspoonful three or four times a day. 


Adrenalin.— During recent years adrenalin has been used quite 
extensively for hemoptysis. It has been stated that it works well in 
cases where it is likely that the hemorrhage is due to the erosion of 
a medium-sized vessel, and that in acute inflammatory conditions 
of the lung it is contraindicated. It increases the heart action and 
contracts the bloodvessels, especially of the intestines, kidneys, and 
spleen, and thus increases the blood-pressure. But Gerhardt says that 
the bloodvessels of the lung are but slightly contracted, while Frey 
found that in a bleeding lung in a rabbit the vessels dilated and the 
flow of blood was increased after the administration of adrenalin, and 
Macht? found experimentally that it causes a powerful constriction of 
the pulmonary artery. Moreover, according to von den Velden, the 
coagulability of the blood is increased 50 per cent after the subcu- 
taneous administration of the remedy. Clinical experience with this 
drug has not convinced the writer of its efficacy in hemoptysis and it 
has therefore been discarded. 

Ergot.—Ergot has been given in large doses (a teaspoonful of the 
tincture every three or four hours; ergotin hypodermically). But it 
has been conclusively shown that it increases the pressure in the 
lesser circulation, just what we want to avoid. In the writer’s experi- 
ence it has never been of any value; often decidedly harmful. The 
same may be said about digitalis. 

Atropine.—Atropine administered hypodermically, in doses of <5 grain 
every three or four hours, according to indications, has been of more 
service than ergot or digitalis. Still, in some cases the writer has 
observed an increase in the hemorrhage soon after its administration. 

Gelatin.— With a view of increasing the coagulative power of the 
blood, gelatin has been recommended by Dastre and Floresco,’ though 
there is evidence that the Chinese used it as a hemostatic as far 
back as the third century. Four to 6 ounces of a sterilized 3 per cent 
solution of gelatin are injected under the skin of the abdomen or thigh. 
Great care must be taken in preparing the solution, as well as while 


1 Jour. Am. Med. Assn., 1909, 53, 1629. 
2 Jour. Pharmacol. and Exper. Therap., 1918, 3, 243. 
3 Compt. rend de la Soc. de biol., 1896, 3, 243. 


50 


786 SYMPTOMATIC TREATMENT 


injecting it, because severe cases of sepsis, even tetanus, have been 
reported. Altogether it is not a harmless procedure—it is painful, 
leaves painful infiltrations at the site of the injection, often provokes 
fever, and is followed by urticarial eruption. If gelatin is used at all it 
should be given by mouth. ‘The patient may be given jelly made from 
calves’ legs, etc., or gelatin may be mixed with milk; or a concentrated 
solution may be administered per rectum. On the whole, its efficacy 
in pulmonary hemorrhage is problematical. 

Calcium Lactate, Acetate, Chloride, etc., are other time-honored reme- 
dies given with a view of increasing the coagulability of the blood 
in doses of 10 to 20 grains repeated four to six times a day. Their 
utility is doubtful; all that may be said about them is that they are 
painless and harmless. Intravenous injections of a 5 per cent calctum 
chloride solution has been found to stop hemorrhages. The writer 
has tried it in pulmonary hemorrhages, using first small doses; 5 ce 
of the 5 per cent solution, then in larger doses, up to 30 cc. But no 
encouraging results have been attained. 

Camphor.—Several authors have recommended camphorated oil, 
administered hypodermically, in pulmonary hemorrhage. Lunde! 
reports that the hemorrhage stops immediately after the injection of 
3 ce of 20 per cent camphorated oil. In the experience of the writer, 
it is not superior in its effects to emetin, but it should be used in obsti- 
nate cases. 

Blood Serum.—The use of blood serum in hemophilia has suggested 
its application in hemoptysis with a view of increasing the coagulability 
of the blood. Horse serum may be used in doses of from 20 to 40 cc 
subcutaneously. Inasmuch as at present diphtheria antitoxin is 
everywhere available, it may be used. But manufacturing chemists 
now have on the market appropriate preparations. It should not be 
used several times at long intervals for fear of anaphylaxis. I have 
tried it several times and was not favorably impressed with it. 

Thromboplastin and Euglobulin, which have been prepared according 
to A. F. Hess’s method, and found efficacious when applied directly to 
bleeding surfaces, have been tried by George Mannheimer and Stanley 
L. Wang? in the treatment of pulmonary hemorrhage. It appears 
from the published cases that these preparations have no effect on the 
bleeding. 

Venesection.— With a view of producing a rapid fall in the blood- 
pressure, venesection has been used in desperate cases of pulmonary 
hemorrhage. In the days of indiscriminate bleeding, this was one 
of the standard therapeutic measures,’ but even at present many 

1 Norsk Magazin for Laegevidenskaben, 1918, 79, 1253. 

2 Am. Rev. Tuberc., 1917, 1, 469. 

%’ According to Sidney Colvin (John Keats, London, 1917, p. 384), John Keats, the 
youthful but consumptive English poet, was bled when he was frightened one night by 
the expectoration of blood. Keats stated that he could not be deceived in the color, 


which indicated to him that it was arterial blood, and that it was surely his death-war- 
rant. He, however, lived for about twelve months after that pulmonary hemorrhage. 


HEMOPTYSIS 787 


authors recommend it. Bonney recommends it when the blood- 
pressure is abnormally high, even in small initial hemoptysis, and also 
in bronchopneumonia following pulmonary hemorrhage, when the 
right heart is dilated and there are pulmonary edema, cyanosis and 
coma. More recently A. G. Shortle! urged this method again in cases 
in which the bleeding is seriously interfering with the functions of 
respiration. “The prompt relief to the impaired respiration is not 
the only benefit rendered in such cases. The coughing and struggling 
for breath, with the coincident inspiring of blood and sputum into 
the air cells is also stopped, and the development of bronchopneumonia 
may be prevented.” In persisting hemorrhages it is also indicated, 
according to Shortle: “It is safer to bleed from the arm than from the 
lung.” 

Of course, this is rather heroic treatment, and involves great respon- 
sibility, especially when attending to patients in their homes. But in 
desperate cases, in which there is evidently nothing to lose, it may 
be given a trial when everything else has failed. 

Diet in Hemoptysis.—In cases of slight hemoptysis with streaky 
sputum, or when a few mouthfuls of blood are brought up, the diet 
need not be changed. But in active and profuse hemorrhage all solid 
and hot foods are to be interdicted. Inasmuch as the first indication 
is to reduce the blood-pressure, we must restrict the quantity of 
fluids ingested. Sudden or rapid filling of the bloodvessels with water 
increases the blood-pressure and may lead to an increase in the bleed- 
ing. In European resorts, where phthisis is treated with mineral 
waters, hemorrhagic cases have been excluded ostensibly for the 
reason that excessive ingestion of water mduces hemorrhage. In 
very copious hemorrhages, fluids should be given only for the purpose 
of allaying thirst—a couple of ounces at a time. Swallowing small 
pieces of ice serves this purpose best. Alcohol, coffee, tea, etc., 
should be discarded. Milk, eggs, scraped beef, etc., may be given in 
small quantities at a time. 

Twenty-four hours after the cessation of the bleeding, irrespective 
of the clots expectorated with the sputum, we may begin to feed the 
patient guardedly. The general condition of the patient, as well as 
the concomitant symptoms, should be our guides. A cup of milk every 
hour or two, cream, a raw egg, and some scraped beef may be given. 
On the third day ordinary feeding may be resumed, so that about 
five or six days after the hemorrhage a standard dietary is reached. 

Convalescence.—During convalescence, if there is no fever, or there 
are no other complications, the patient may be permitted to sit up in 
bed, or on a comfortable chair twenty-four hours after the cessation of 
active bleeding. The expectoration of clots, which continues for several 
days, as a rule, should not deter us from allowing the patient to sit up. 
Forty-eight hours after the stoppage of active bleeding I permit my 


1 Tr. Nat. Assn. Study and Prevent. of Tuberc., 1915, 11, 147. 


788 SYMPTOMATIC TREATMENT 


patients to walk around the room. I have not met with a case in which 
walking induced a new attack of hemorrhage. On the other hand, the 
resumption of exercises should be delayed, especially after profuse 
hemorrhages. The patient is more or less exsanguinated and weak. 
He needs rest and good nourishment to recoup. It is best that for two 
or three weeks after such a hemorrhage the patient should keep at 
comparative rest. The cough should be carefully controlled during 
that period and exposure, especially to intense sun rays, avoided. 

Dyspnea.— We have seen that subjective dyspnea is rare in uncompli- 
cated chronic phthisis, and that the patients are only rarely short- 
winded, if at all. In some cases this symptom demands treatment. 

Toxic dyspnea, due to progressive disease of the lung, is best treated 
by rest. It is always accompanied by fever, and the treatment directed 
to remove the pyrexia usually helps along in the direction of relieving 
the air hunger. During acute exacerbations in the course of chronic 
phthisis, toxic dyspnea is very frequent and the treatment is clearly 
defined. 

Dyspnea is often due to some preéxisting disease. This is the case 
with pulmonary emphysema, asthma, cardiac and renal disease. The 
treatment is that of the underlying pathological condition. In those 
having emphysema, or asthma, the iodides are very often of immense 
help, provided there is no tendency to hemoptysis. For the nocturnal 
attacks of dyspnea, morphine or heroin may have to be given. 

Dyspnea may be due to some acute or subacute complication, such 
as pleurisy, with or without effusion, spontaneous pneumothorax, 
etc. The treatment is considered in the sections dealing with these 
complications. In the terminal stages of the disease the air hunger 
may only be relieved by large doses of morphine or heroin, and no 
patient should be denied these solacing remedies. The danger of 
habit formation should not be thought of at this stage of the disease. 
The severe dyspnea and cyanosis is here due to weakness of the 
atrophied respiratory muscles, limitation of the lung area owing to 
extensive destruction of the parenchyma, and, most commonly, to 
miliary invasion of both lungs with tubercles. The prognosis is 
hopeless. 

Cardiac Weakness.—Patients who suffer from tachycardia or car- 
diac palpitation, permanent or provoked by mild exertion or excite- 
ment, must be kept at perfect rest in bed, and all forms of nervous 
and emotional excitement are to be avoided. At times these cardiac 
disturbances are due to gastric derangement and may call for modi- 
fications in the quantity and quality of the food. 

In many cases, especially in the advanced stages, palpitation is due 
to cardiac displacement, especially in left-sided lesions in which the 
heart is drawn upward and to the left. Rest is the only remedy we 
have for this condition. 

From whatever cause cardiac weakness arises, it may at times 


PAINS IN THE CHEST 789 


become acute; collapse is not uncommon after some excitement or 
overexertion. Now and then a patient dies suddenly as a result of 
heart failure. For collapse, hot drinks of whisky, warm applications 
to the extremities, and some stimulants like camphor, strychnine, etc., 
are to be administered hypodermically. 

In the far-advanced stages there is acute dyspnea, cyanosis, and 
edema, owing to cardiac failure resulting from the extensive lesion, 
toxemia, etc. These terminal symptoms are treated with digitalis, 
though in my experience this drug has only exceptionally an influence 
on the heart at this stage. In most cases the subjective feeling of weak- 
ness and air hunger are best relieved by liberal doses of morphine or 
heroin. 

Insomnia.—In phthisical patients insomnia may be due to various 
causes, and it is not advisable to resort to soporific medication in every 
case. Rest and fresh air in the sleeping room may induce sleep; 
so may avoidance of a heavy meal late in the evening, a warm bath 
before retiring, etc. These means will suffice in most of incipient 
cases in which the sleeplessness is due to worry on account of the 
seriousness of the ailment. In some of these cases the bromides are 
very useful. 

In incipient cases Insomnia may be due to the cough which keeps 
the patient awake, and the indications are those discussed when speak- 
ing of the treatment of cough. When due to digestive disturbances, 
it is to be treated accordingly. In the advanced stages it is often 
due to the fact that the patient is lying at perfect rest during the 
whole day, and sleeps several hours, for an hour or so at a time. The 
patient is then to be kept awake during the day. In some cases 
hypnotic drugs must be given, and of these sulfonal or trional, in 10- 
to 15-grain doses, may be administered; 3 to 6 grains of veronal will 
serve the purpose in some cases. If the treatment has to be prolonged, 
the drugs may have to be alternated. In the far advanced stages only 
large doses of morphine may give relief. 

Pains in the Chest.—Most of the pains in the chest complained of 
by tuberculous patients may be relieved by the administration of some 
placebo, or the application of a mustard plaster, dry cupping, tincture 
of iodine, ete. In some cases it is necessary to administer some of the 
coal-tar analgesics or salicylates. Small doses of antipyrin, phenacetin, 
pyramidon, ete., with caffein may be given. Sodium salicylate or 
aspirin gives relief in many cases. But in rare instances we meet 
with patients in whom the pains in the chest are so severe as to require 
the administration of a dose of codein or morphine. When due to 
intercurrent pleurisy, strapping of the chest with adhesive plaster is 
indicated. The pains in the shoulder, often due to diaphragmatic 
pleurisy, which are very acutely felt especially during the night, are 
very difficult to manage. The coal-tar analgesics and the salicylates 
usually give no relief, and often even safe doses of morphine fail. Hot 


790 SYMPTOMATIC TREATMENT 


applications to the affected part, or, rarely, the actual cautery, may be 
necessary. 

Anorexia.— Many patients have a good appetite; even when the 
fever is comparatively high the desire for food may be retained, 
which is not observed in other febrile diseases. But in others it is 
defective or inadequate to induce them to ingest a sufficient quantity 
of food for the replenishment of the inroads on their bodies made by 
the disease. It has been my experience that their number is not very 
large among those who are well instructed along the line of proper 
food and nourishment. 

Medicinal treatment is not the first thing to give in anorexia. Out- 
door life, regulated exercises, regularity of meals, etc., suffice in most 
cases to improve the appetite to the desired degree. In many it will 
be found that dietetic errors are at the bottom. The traditional and 
stereotyped advice, “plenty of milk and eggs,” given indiscriminately, 
is more responsible for disgust for food than any other single factor. 
Drinking two or even three quarts of milk a day, and swallowing 
six to twelve raw or soft-boiled eggs, overload and often dilate the 
stomach, produce congestion of the liver, and create a disgust for 
all kinds of food. While some patients, who may be considered 
dietetic curiosities, may keep up with such a régime for weeks and 
even gain in weight, in the vast majority the digestive organs revolt, 
the palate loses its taste for food altogether and, coupled with diarrhea 
or constipation, the functions of assimilation fail. 

In this class of patients we may note with satisfaction a remarkable 
change soon after the quantity of milk and eggs is reduced, or they are 
altogether discarded for a time. We must never neglect to tell our 
patients that so long as the appetite and digestion are good, they need 
not make any changes in their accustomed diet, excepting perhaps to 
increase the quantity, which is very desirable. With a variety of food- 
stuffs it is usually easy to consume more than before the onset of the 
disease. Instructions along the lines of good cooking should never be 
neglected. Among the poor and moderately well-to-do it has been my 
habit to send for the mother, wife or sister of the patient and urge her 
to exercise special care in the preparation of the food and to cater to 
the palate of the patient. The person who has prepared food for the 
patient for a long time knows best what he will relish. Of course, the 
teeth are to be examined and repaired in case caries is found, and 
proper instructions as to mastication are to be given. 

In most cases the appetite can be improved by corrections of any 
of the just-mentioned errors without any medication at all. All are 
to be told in plain language that their only chance for recovery lies 
in consuming proper food and plenty of it; that they can best be cured 
through their stomach, and that they must eat even if the desire for 
food is not at its best. This often has the desired effect. When the 
patient finds that with proper food he gains in weight he is encouraged 


GASTRIC DISTURBANCES 791 


to eat more. The gain in weight is usually seen best during the first 
month or two, but after a considerable increase the gain slackens. 
So long as he holds his own at his former weight, or little above, there 
is nothing to worry about. 

Very frequently superalimentation is the cause of anorexia. In 
these cases it is advisable to try C. V. Spivak’s! suggestion: The 
patient who lacks an appetite is told to omit one, two or more meals 
until the appetite naturally returns. Natural hunger, thus induced, 
at times improves the appetite and relish for food much better than 
any dietetic or medicinal procedure. 

Gastric Disturbances.—In some cases we must resort to medication 
to provoke an appetite. I consider creosote as the drug which acts 
the best. Small or moderate doses of creosote or any of its derivatives 
—creosote carbonate, guaiacol, guaiacol carbonate, etc.—may be 
given and the appetite and digestion promptly 1 improve. In others 
we may give bitter tonics—the tinctures of nux vomica, condurango, 
cinchona, ete. Orexin tannate is also good in 5-grain doses i in powder 
or tablet form taken half an hour before meals. When there is diar- 
rhea this drug is very good. I have used the following with good 
results: 


- 


R—Tinct. nucis vomice . Re a) eae ahh ll 8.0 
Acid. nitrohydrochlorici Shiva ae: hee ae LY 12.0 
Tinct. gentianz comp. ee Ce : 5ij 64.0 
Tinct. cardamomi comp... ‘ a. 3. ea Ziv 120.0 


i] 


M. 8.—One teaspoonful well diluted i in water three times a day before mica!s. 


The nux vomica may be replaced by condurango, and the nitro- 
hydrochloric acid’ omitted, in cases in which they are contraindicated. 
In obstinate cases stomachic medicaments are to be changed often. 

In hyperacidity dietetic changes are to be made according to indica- 
tions, and it is always to be borne in mind that it may be due to 
overfeeding. Often medication is necessary. I have had good results 
with the following: 


R—Magnesii oxidi 5 wets £o, Tee “pects ee sree 3h 16.0 
SOCMADICATDONAtLSEES H4noe eh ee ee 32.0 
Emiraciibelladonmegaemes Snare Sie use fn). 0c) PT.1) Osis 


M. ft chart. No. xxiv div. 
S.—One powder three times a day after meals. 


Or the following effervescent powder may be given: 30 grains of 
bicarbonate of sodium in one powder, and 10 grains of tartaric acid 
inanother. Each of these is to be dissolved in half a tumbler of water, 
then added one to the other and swallowed during effervescence. 
Some are relieved by a tablet of ;4 5 grain of atropine sulphate given 
after meals. 


1 Colorado Medicine, 1918, 15, 90. 


792 SYMPTOMATIC TREATMENT 


Constipation.— Constipation is another of the troubles of the phthis- 
ical which often interferes with the favorable progress of the case. 
It is best combated by proper dietetic measures, especially increasing 
the quantity of fruits and vegetables, fresh and cooked. But mildly 
laxative drugs must be given in many cases. Before giving them 
we must make sure that it is not one of the anodyne drugs, codein, 
morphine, dionin, ete., which is responsible. Phenolphthalein appears 
to be the best, and 3 to 5 grains may be given, and next to it cascara 
sagrada in appropriate doses. 

In the advanced stages, complicated by adhesive peritonitis, when 
diarrhea is apt to alternate with constipation, laxative drugs are to 
be used with caution. They may induce uncontrollable diarrhea. It 
is always better to first try proper changes in the diet, or the effects 
of some special food. Thus, I find that buttermilk will cause a move- 
ment of the bowels better than any medication in some tuberculous 
patients. 

Diarrhea.—We have seen that diarrhea in the tuberculous is not 
always due to ulcerations in the intestines and that the latter may 
exist while the patient is constipated. In many cases the diarrhea is - 
due to chronic catarrh of the bowels induced by swallowed sputum, 
and the patient is to be warned against this very bad habit. In 
others it is due to consumption of large quantities of raw milk, and 
particularly raw eggs, as has already been shown (see page 741), and 
this must be corrected. 

In case the diarrhea is due to tuberculous ulceration or amyloid 
degeneration of the intestines, it is often very difficult to manage. 
The patient must remain in bed and appropriate changes be made 
in the diet. Fluids in general are to be reduced in quantity, especially 
cold drinks. The great majority of vegetables, salads, fruits—raw or 
cooked—pastries, rye bread, fats and sweets are to be avoided. While 
most patients tolerate milk very well, there are many who do not and, 
in obstinate cases, it is advisable to discard it for a few days and watch 
the effects. Bouillon and soups should be given without the addition 
of vegetables; eggs, butter, scraped or finely minced beef, boiled 
fish and oysters may be allowed, but no lobster. Of the vegetables 
and cereals allowed the following may be mentioned: rice, sago, 
etc., boiled in milk or served with cream, mashed potatoes, ete. 

In many cases medicinal treatment must be given to control the 
frequent stools. The ancient “‘styptic’’ remedies, such as lead acetate, 
iron, alum, etc., are worthless in the vast majority of cases. But the 
modern preparations of tannin, such as tannigen, tannalbin, etc., are 
occasionally of service in large doses, and should be given a trial. The 
subnitrate of bismuth should be given in doses of 10 to 15 grains five 
or six times a day. But in most cases optum must be used, more or 
less. Bismuth or tannigen may be given in powders combined with 
fairly large doses of Dover’s powder, or the official tincture of opium 
in 5- to 10-minim doses three or four times a day. 


DIARRHEA 793 
R= annivcnie wa ae eee one ne on et eto K1y 1220 
VeyeraAdavelervingwney 4 6 « © 6 o 8 oc 9 Oia 24.0 
FCGSOLCINIG Is maNnre ne ame amen ee Pr eee OTS, 1K 0.6 
M. ft. cachet No. xviii. 
$.—One cachet four times a day. 
R—-Bismuthi submitratis 40.9 5.) oe Od 32.0 
Tinct. opii deodorati . AN a oe The ee eee i 8.0 
Aqueze cinnamoni . . . ab) Oe se ad. ea Ly. 120.0 


M. 8.—One teaspoonful four times a day. 


When bismuth subnitrate fails we may try the subgallate in 10- to 
15-grain doses with or without opium. There are, however, many 
cases in which everything, even the administration of heroic doses 
of opium fails to stop the diarrhea, and we must be content with 
relieving the pains. 

D. Mandl has had good results in rebellious diarrhea by the injection 
into a vein in the arm of 5 cc of a 5 per cent solution of calcium 
chloride. Saxtorph! reports encouraging results with this method and 
says that a large proportion of patients are freed from the symptoms 
of intestinal tuberculosis for quite a long time. A rather extensive 
experience with this mode of treatment has convinced the writer that 
only in a certain class of cases it has proved of value. When the diar- 
rhea in a tuberculous patient is due to dietetic indiscretions, to catarrhal 
conditions of the mucous membrane, or to slight intestinal ulcerations, 
an intravenous Injection of 5 cc of a 5 per cent solution of calcium 
chloride will give prompt and prolonged relief. In some cases it is 
necessary to repeat the injection once or twice at three-day intervals. 
In many cases the pains in the abdomen are relieved much earlier than 
the loose stools. On the other hand, when the abdominal pains and 
diarrhea are due to extensive ulcerations of the intestine, and amyloid 
changes in the mucous membrane, very little can be expected from this 
mode of treatment. Likewise, afebrile cases are more often benefited 
than those with fever. 

Some of these patients complain of tenderness or pain in the abdo- 
men. ‘This is best relieved by hot fomentations. In the later stages, 
when emaciation is extreme, the extremities are to be kept warm and 
the unfortunate patient should not be denied the merciful relief of 
morphine in large doses. 


1 Ugeskrift for Laeger, 1918, 80, 1763. 


CHAP TER bev. 


OPERATIVE TREATMENT—ARTIFICIAL 
PNEUMOTHORAX. 


Historical Note.—Tuberculous pneumothorax has been the most 
dreaded of complications of phthisis and experience has taught that 
the vast majority of patients who suffer from this accident succumb. 
But some have observed that a pneumothorax may be what the 
French call “providential,”’ and exert a rather salutary influence on 
the symptoms of the underlying disease. In a very interesting study 
of the physiology of respiration James Carson! suggested that the most 
rational treatment of phthisis would be collapse of the affected lung. 
So convinced was he of its possibilities, that he induced two patients 
to submit to the operation. The first was ‘James, Sloane Esq., an 
eminent merchant of Liverpool, the last of five brothers, the other four 
having died of consumption a few years before, who had returned from 
the West Indies, to which he had gone for the purpose of trying what a 
change of climate might do in his case, in the last stage of consumption, 
which he knew to be incurable from any known remedies. Soon after 
his return he heard of the paper to which I have alluded and soon 
became determined of having the operation which I suggested as a 
possible means of giving relief, performed in his own case. It was 
done on the 26th of September, 1822, by Mr. Bickersteth, an eminent 
surgeon of this place, in the presence of the late Dr. McCartney and 
myself. An incision calculated to admit air freely into the chest was 
made between the sixth and seventh rib. As the sound usually heard 
upon an opening being made into the chest, and produced no doubt 
by the rapid passage of the air through the opening was not perceived 
in this case, it was suspected that the lung did not collapse, and that an 
adhesion prevented the entrance of the air. It was not deemed advis- 
able to make a further examination at this time.” A second patient 
who submitted to a similar experimental operation also had pleural 
adhesions which prevented the entry of air into the pleural cavity. 
Carson’s suggestion was forgotten for many years, though we find it 
mentioned in various books dealing with tuberculosis published during 
the first half of the nineteenth century. In his book on diseases of the 
chest, published in 1837, that acute clinical observer, William Stokes,? 


1 An Inquiry into the Causes of Respiration; of the Motion of the Blood; Animal 
Heat; Absorption; and Muscular Motion; with Practical Inferences, second edition, 
London, 1833. 

2 Treatise on Diseases of the Chest, New Sydenham edition, p. 455. 


PRINCIPLES UNDERLYING THE TREATMENT 795 


has this to say: ‘‘The proper symptoms of phthisis are in many cases 
arrested, and singularly modified, by the occurrence of the new disease 
(pneumothorax). I have often found that after the first violent symp- 
toms had subsided, the hectic ceased, the phthisical expression dis- 
appeared, the flesh and strength returned; and in this way the patient 
has enjoyed many months of comfortable existence, and was only 
disturbed by dyspnea and the sound of fluctuation on exercise.” 
In his book on Diseases of the Lungs, published in 1860, Walter Hayle 
Walshe! says: “In some recorded cases of actively advancing phthisis, 
the first sufferings of accidental perforation having passed, it has 
certainly appeared, though the signs of hydropneumothorax remained, 
that the phthisical symptoms themselves underwent improvement. 
But an occurrence so rare gives no warranty for the fanciful proposal 
to treat phthisis by producing artificial pneumothorax.” This shows 
clearly that the method was suggested in England long before Forlanini 
had done it in Italy. During the course of the nineteenth century 
many other physicians have reported experiences similar to those of 
Stokes and Walshe just quoted. 

It was, however, C. Forlanini,? of Pavia, who first induced a pneumo- 
thorax for therapeutic purposes, and reported his experiences in 1894. 
Independently of Forlanini, John B. Murphy,’ of Chicago, did the 
same in 1898. But for some time no notice was paid to this method 
of treatment until Brauer, Spengler, and some others, took it up in 
Germany. At present it is one of the recognized methods of treat- 
ment of certain cases of pulmonary tuberculosis. That zt is a valuable 
method will be appreciated when it 1s borne in mind that vt 1s mostly 
indicated in cases in which everything else has been tried and found 
wanting; in other words, when there is everything to gain and nothing 
to lose. Contrasted with other methods of treatment, which are 
nearly always stated to exercise their alleged curative effects only 
during the incipient stage of the disease, when diagnosis is often 
doubtful, and spontaneous cures are not uncommon, it is to be consid- 
ered one of the best therapeutic procedures we have at present for 
the cure of phthisis. 

Principles Underlying the Treatment.— The aim is to introduce into 
the pleural cavity a sterile and harmless material which will collapse 
the lung in the affected, or more affected, side of the chest. The lung 
is thus put at rest and given an opportunity to heal. We have already 
seen that functional rest is as important in phthisis as in other diseases. 
In surgical tuberculosis rest has been more effective as a curative agent 
than all other methods. Rest has also been used with beneficial 


1 Practical Treatise on Diseases of the Lungs, American edition, Philadelphia, 1860, 
p. 250. 

2 Gazz. d. osped., 1882, 3, 537, 585, 601, etc.; Gazz. med. di Torino, 1894, 65, 381, 401. 
For a complete summary of Forlanini’s work on this subject, see Forlanini, Die Behand- 
lung der Lungenschwindsucht mit dem kiinstlichen Pneumothorax, Ergebn. d. inneren 
Medizin u. Kinderheilkunde, 1912, 9, 621-655. 

3 Jour. Am. Med. Assn., 1898, 21, 151, 208, 281, 341. 


796 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


results in other diseases, notably general rest in functional nervous 
diseases, as was worked out by Weir Mitchell; tracheotomy in certain 
laryngeal conditions, gastro-enterostomy in cancer, and especially in 
ulcer of the stomach, enterostomy in certain diseases of the lower 
bowels and rectum, ete. 

The lung is one of the organs of the body which never rests but 
expands and contracts at least 12,000 times per day throughout 
life. With an artificial pneumothorax we can place one lung at rest 
almost as effectively as the splint puts at rest a- tuberculous joint, 
without endangering the life of the patient. Moreover, the lung is 
the only organ in the body which is.constantly in a state of distention. 
Even after the most forced expiration it does not collapse utterly. 
Any solution in continuity in the pulmonary tissues remains separated 
and there appears to be no tendency to bring about the union of the 
diseased parts, or to facilitate the process of healing, by coaptation. 
Inflating gas into the pleural cavity and collapsing the lung, we achieve 
two objects: The lung is immobilized at its root, and it is compressed 
by the gas in the pleural cavity and the retraction of its elastic tissues. 
Its volume is greatly reduced, diseased parts and walls of cavities are 
brought into apposition, so that they may cicatrize by the formation 
of connective tissue. 

Pneumothorax does even more than afford rest to the diseased lung. 
By compression it empties the lung of its contents. The pus and cheesy 
detritus in cavities, the inflammatory exudates in the alveoli and 
bronchioles are all squeezed out as from a sponge, removing the main 
source of toxic absorption. It also limits the diseased focus and pre- 
vents its spread, so that the healthy parts of the lung remain so while 
the lesion is in time converted into a cicatrix, or is encapsulated. As 
a result of drainage, mixed infection is eliminated and prevented. The 
fact that the air current entering through the trachea cannot circulate 
within the collapsed lung tissues prevents superinfection of healthy 
parts of the organ with emboli of detritus carried from one part to 
another along the bronchial tree, and mixed infection with micro- 
organisms other than tubercle bacilli, which may be brought in with 
the air current, is avoided. 

The circulation of the blood is impeded in the collapsed lung, but 
there occurs a venous or passive hyperemia which is known as an 
important factor in the defence of tissues against tubercle bacilli. The 
comparative protection against tuberculosis enjoyed by cardiacs is 
ascribed by some authors to the venous hyperemia of the lungs. The 
lymph channels of the collapsed lung are compressed, as has been 
shown by Shingu,! who subjected animals with induced pneumothorax 
to the inhalation of soot, and at the autopsy found that the collapsed 
lung remained free from soot. Animals were compelled to inhale 
large quantities of soot, and subsequently pneumothorax was induced, 


1 Beitr. z. Klinik. d. Tuberkulose, 1908, 11, 1. 


TECHNIC 797 


and when they were finally killed it was found that the free lung was 
darker than the collapsed lung. This tends to show that the circula- 
tion of lymph, which is the main factor in removing inhaled particles 
from the lung, is impeded or arrested because of stasis of lymph in 
the compressed lung. In this manner the absorption of toxins from 
the lesions into the general circulation is impeded or arrested in 
pneumothorax, the clinical phenomena of phthisis, such as fever, 
nightsweats, weakness, etc., are prevented, and the body is thus given 
an opportunity to recuperate. Moreover, the lymph stream being 
unable to carry away bacilli from the lesion, the process is localized 
to the affected areas. These points have been found clinically, at the 
autopsy table, and experimentally. 

Technic. —The technic of the induction of a pneumothorax is simple, 
but not devoid of danger and even fatal accident. The object is to 
inject gas into the pleural cavity and not anywhere else. Forlanini 
developed a technic which is both painless and bloodless. Murphy, 
without knowledge of Forlanini’s work, developed a_ practically 
similar technic. Brauer was not satisfied that the Forlanini-Murphy 
method is safe and advocated the open incision method. 

The Brauer Method.—This consists in incising the chest wall, dissect- 
ing down to the pleura by cutting through the fascia, and separating 
the intercostal muscles with a blunt instrument in the direction of 
their fibers. When the parietal pleura is exposed, it is punctured 
with a blunt needle or cannula, and the gas is allowed to flow in by 
aspiration of the pleural cavity or by pressure, when indicated. This 
method has failed to get many adherents for many reasons. But 
few patients want to submit to a cutting operation. Then there is 
an obvious danger of sepsis which may, of course, be avoided by the 
usual methods. I have found no reason for resorting to the bloody 
operation, and feel confident that if this was the only available method 
of inducing an artificial pneumothorax we should find very few patients 
willing to submit. 

Very few now practice this open incision method, and most of those 
who do it make use of it only occasionally when the Forlanini method 
fails because of pleural adhesions. It is however, a fact that when the 
Forlanini method fails, the open incision almost invariably fails to 
find a non-adherent pleural sac. 

The Forlanini-Murphy Method.—It consists in a simple, bloodless 
puncture of the chest wall with an especially constructed hollow 
needle which is connected with a gas reservoir and a water manometer 
through a T-shaped tube. When the lumen of the needle punctures 
the costal pleura the gas is allowed to flow into the pleural cavity by 
the suction or negative pressure in that cavity, as well as by some 
positive pressure which must, at times, be used at the gas reservoir. 

Simple as this operation appears to be, there are certain difficulties 
to be overcome and dangers to be avoided. The main difficulty is to 
pass the needle as far as the costal pleura, puncture it, and avoid pene- 


798 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


trating the visceral pleura and the lung. The dangers are mainly in 
allowing the gas to flow into places other than the pleural cavity, 
especially into a bloodvessel, thus causing gas embolism, which while 
not invariably fatal, yet is sufficiently menacing to be dreaded by all 
who are doing this sort of operation. 

No special preparation of the patient is indicated. Brauer and 
Spengler! do not perform it in women during the menstrual period; 
Saugman avoids even the premenstrual period. 




















Fic. 120.—Robinson’s modification of the Brauer apparatus for inducing pneumothorax. 


Apparatus.—T'o avoid accidental entry of gas into bloodvessels or 
any other tissue but the pleural cavity various forms of apparatus 
have been invented. As is usual, they are all based on one main 
principle—the manometer which was introduced by Saugman. Each 
apparatus consists primarily of two graduated bottles connected 
by tubing, one containing the gas to be injected, and the other some 
fluid, so that the fluid flows from its container into the other bottle, 
displacing the gas which is sucked or pressed into the pleural cavity 
through a tube and an especially constructed needle. This last- 
mentioned tube is T-shaped, or provided with a three-way stopcock, of 


1 Handb. d. Tuberkulose, 1919, 3, 192. 


seavesed tent ttcasteasiti a 





















































‘e222 Sa es 
THE KNY SCHEERER CO. 


Fic. 121.—Forlanini-Saugman-Muralt apparatus for the induction of pneumothorax. 
This apparatus consists in the main of two glass tubes, twenty-four and a half inches high 
and about two inches in diameter and a U-shaped manometer tube, the latter filled with 
an alcoholic solution of methylene blue and mounted in the center of the board in front of 
a graduated porcelain scale. The two large tubes are joined by means of rubber tubing 
under the base A. The tube to the left is graduated to 1000 ce and the other is plain. 
They are filled with water up to 500 cc. The graduated tube to the left is filled from the 
tank with the gas to be introduced into the pleural cavity, and the gas displaces the water 
which rises correspondingly in the large plain tube to the right. When filling the appa- 
ratus with gas, the rubber tubing from the tank is to be connected with a rubber gas-bag 
to the opening below the stopcock C. Stopcock D should stand vertically. Stopcock 
C should be turned so as to connect through the filter and into the graduated cylinder. 
Stopeock # on the top of the non-graduated tube should be turned so as to allow the 
air in this tube to escape when the gas forces the water into it. When the graduated 
cylinder is full of gas, stopcock C’should be closed. Funnel F connected with the manom- 
eter tube serves for the filling of the manometer tube to zero with an alcoholic solution 
of methylene blue. The graduated glass tube is connected with the glass tube B which 
is filled with sterilized gauze and serves as a filter. The three-way stopcock C connects 
with the manometer as well as the gas cylinder, thus showing the oscillations when the 
needle is in the pleural cavity. When stopcock D is turned horizontally it permits the 
manometric reading showing the degree of oscillation while the gas is still flowing. After 
the needle has been properly inserted into the pleural cavity and stopcock C turned to 
the graduated tube, the gas will be forced out by the weight of water which is contained 
in the plain tube. When extra pressure is required, a small rubber tube is connected 
with the plain tube, so that the remaining water may be gently forced into the grad- 
uated tube. The manometric scale is divided into 50 centimeters, 25 above and 25 
below zero, indicating respectively negative and positive pressure. 


800 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


which one limb communicates with the gas bottle, the second with the 
needle, and the third with the manometer. At any moment during 
the operation we can open or close the tube leading to the manometer 
or the gas reservoir. 

As has been said, all the instruments for the induction of a pneumo- 
thorax are constructed on this simple principle, but it is amazing how 
some have succeeded in complicating them by adding various attach- 
ments which make them unwieldy, and easily disordered. The uni- 
versal experience that a machine in order to be successful must be of 
the simplest construction consistent with efficiency, holds good here. I 
have been using Forlanini’s apparatus as modified by Saugman! and 
von Muralt,? (Fig. 121) and also the Robinson apparatus (Fig. 120). 

The Function of the Manometer.—The entire safety of the operation 
lies in the manometer which has been called by Edward von Adelung? 
the heart of the apparatus. While the needle passes through the skin, 
subcutaneous tissue, muscles, and fascia before piercing the costal 
pleura, the manometer records atmospheric pressure, but as soon as 
it enters the pleural cavity the air in the connecting tube becomes 
rarefied, because the vacuum in the pleural cavity aspirates its air 
content, and the fluid in the closed limb of the manometer is sucked up 
toward the needle, 7. e., from the open into the closed limb, and a dis- 
tinct difference in the levels of the fluid is evident. Moreover, when 
the lumen of the needle is really in the pleural cavity, the respiratory 
movements of the lung are recorded in the manometer which shows 
distinct oscillations of the levels of its fluid. 

This explanation of the work of the manometer, which is found in 
most works on the subject, is unsatisfactory. The fact is that normally 
there is no pleural cavity at all because the parietal and visceral pleura 
lie tightly, one on another; nor can we speak of negative pressure 
between the two pleural sheets because the word “pressure” is here used 
in the sense of gas pressure which can be measured with a manometer; 
but such a negative pressure does not exist between the two pleural 
sheets. The manometric readings, when the lumen of the needle is in 
the pleura, are better explained by Brauer, Piéry,* and Moritz,> and 
especially elaborated by Rist and Strohl,6 in the following fashion: 
The lung must be considered as an organ fixed at its root, and kept in 
a state of equilibrium by the pressure of the atmospheric air within the 
air passages, and by the elastic tension of its tissues. There is a con- 
stant tension of the lung from the roots to the periphery at the thoracic 
walls. The force of this traction is equal to the absolute elastic tension 
in the given direction, minus the atmospheric pressure which prevails 
within the air passages and so prevents its collapse, or retraction, from 

1 Beitr. z. Klinik d. Tuberkulose, 1914, 31, 571. 

2 Ibid., 1910, 18, 359. 

3 Jour. Am. Med. Assn., 1914, 42, 1914. 

4 La pratique du pneumothorax artificiel en phthisiothérapie, Paris, 1912. 


5 Miinchen. med. Wehnschr., 1914, 61, 1321. 
6 Annales de Médecine, 1920, 8, 233. 


TECHNIC S01 


the periphery to the hilus. The intrapleural pressure, therefore, never 
differs much from the atmospheric pressure, as has been shown by 
W. Parry Morgan,! and in consequence any gas drawn into the cavity 
will not be appreciably rarefied. The volume of gas which will have 
passed from the connecting tube into the pleural cavity will be prac- 
tically equal to the amount of fluid which will have passed from the 
open to the closed limb of the manometer. This volume would, when 
the negative pressure stands at 15 cm. of fluid in a manometer tube of 
0.3 em. bore, measure less than 1 ce. 

This is enough to separate the sheets of the pleura, if there are no 
adhesions. But, owing to the elastic tension of the lung and the 
atmospheric pressure within the air passages, there is actually shown a 
negative pressure in the manometer. A little reflection will explain why 
this negative pressure will be stronger during inspiration because of 
the greater distance at that period between the root and the periphery, 



































Fia. 122.—Brauer-Floyd-Robinson needle. 


and less during expiration. With the increase in the quantity of 
gas introduced into the pleural cavity the tension of the lung will 
obviously decrease and with it the negative pressure, until finally a 
point is reached when the pressure in the gas-contaiming pleural cavity 
is 0 and later even becomes positive. 

Bearing in mind these simple principles of the manometer, we are in 
a position to guard against the most important of the accidents which 
are liable to happen during the operation. In patients with pleural 
cavities free from adhesions, ordinary and careful attention to the 
manometer will suffice to guard against mishaps. ‘The manometer 
shows conclusively whether the lumen of the needle is in the pleural 
cavity or not. It also gives reliable information as to the state of the 
pleural cavity with particular reference to adhesions, showing whether 
they are dense and extensive, or of slight extent and may be separated 
and broken up by an increase in the intrapleural pressure with the gas. 


1 Lancet, 1914, 2, 90, 
ol 


802. OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


During the course of the treatment we are able to ascertain, with the 
aid of the manometer, whether the nitrogen has been absorbed and a 
refill is necessary; whether the lung has been completely immobilized 
or has remained expansile. When it is found that the intrapleural 
pressure increases, and this cannot be attributed to excessive gas 
insufflations, it indicates pleural effusion. The difficulties in cases 
with pleural adhesions will be discussed later on. 

The Needle.— Various, some rather complicated, needles have been 
devised for this operation. The fact is that any trocar and cannula 
may serve the purpose; in fact, an ordinary hypo- 
dermic needle has been used successfully. For 
the first operation it is, however, best to use one 
with an obturator, which prevents the admission of 
air, an arm right below the obturator, to which 
the tube leading to the gas bottle and manometer 
is attached. As is stated elsewhere, the needle 
supplied is usually too long; one a little more 
than one inch in length is best. For the first 
operation the gauge may be over 1 mm., but for 
subsequent refills, especially in patients showing 
high suction of the pleura, the gauge should be 
from 0.4 to 0.8 mm. at most. Subcutaneous 
emphysema is often the result of thick needles. 

The Gas Used for Inflation—Because it was 
supposed that when oxygen is injected into the 
pleural cavity it is quickly absorbed, and that 
nitrogen will remain within that cavity for a 
longer time, this element was selected and most 
operators use it. But further experience has 
shown that atmospheric air is just as good. Webb, 
Gilbert, James and Haven,! Tobiesen? and espe- 
clally Tachau and Thilenius* and Rist and Strohl,4 
have shown clinically and experimentally that 
nitrogen has little if any advantage over atmos- 

lid: Wigs Senos pheric air, because in either case diffusion of gases 
Lined. occurs so rapidly that within a few hours the 

proportion of the two gases, nitrogen and oxygen, 
is about the same. For this reason there is no necessity for using 
nitrogen. Air does just.as well. Nitrogen is rather expensive when 
bought in tanks from manufacturers, and while most of the apparatus 
for the production of pneumothorax is portable, the large iron tank of 
nitrogen is not easily transported, and atmospheric air is to be given 
preference in private practice. 





1 Arch. Int. Med., 1914, 14, 883. 

2 Brauer’s Beitrage, 1911, 21, 109. 

3 Ztschr. f. klin. Med., 1916, 82, 199 and 282, 
4 Annales de Médecine, 1920, 8, 233, 


TECHNIC 803 


The Selection of the Point for Injection.—The first inflation must be 
carefully done, and it is important to select a point to introduce the 
needle where no adhesions are likely to be encountered. Bearing in 
mind the anatomy of the chest and its viscera, it is evident that the ideal 
point is between the anterior and posterior axillary lines, in the fourth 
to the sixth intercostal spaces. Here pleural adhesions are com- 
paratively uncommon, and in left-sided lesions the needle is not likely 
to plunge into the heart, a complication which has occurred twice in 
the hands of a very skilful operator. It must be mentioned that this 
accident proved harmless ultimately, though the immediate effects 
were threatening. When the patient lies on the opposite side and 
draws his arm above the shoulder, the intercostal spaces are widened, 
and the tissues hardened so that the needle passes easily through, 
obviating the use of force. But because at the mentioned region the 
interlobar fissure reaches the periphery, there are apt to be adhesions 
at the fourth or fifth intercostal spaces, and for this reason it is best to 
try first the seventh or eighth interspace, where the chances of entering 
the pleural cavity are better. When the lesion is mainly in the lower 
lobe, or there are unmistakable signs of pleural adhesions over the 
lower lobes, the puncture should be made in one of the upper, the third 
or fourth interspaces. Of course, when we are free to choose, areas 
covered with thick muscles, or the thick mammary gland in women, are 
to be avoided. But we are not always free to choose, and any point 
must serve our purpose when the elective places are not available 
because of adhesions. It must also be emphasized that it is very diffi- 
cult, often impossible, to avoid pleural adhesions with all the means 
of diagnosis at present at our command. 

We are generally guided by the following principles: The chest 
is punctured as far as possible away from the main pulmonary lesion 
because pleural adhesions are most likely to be encountered over 
the diseased lung and, what is more important, while puncturing 
the lung is ordinarily harmless, in such places the needle may, how- 
ever, penetrate a cavity and produce a pyothorax. But adhesions 
are found everywhere, and often where we least expect them. Physical 
diagnosis is apt to prove misleading, and the fluoroscope and roentgen- 
ography just as often may fail to reveal them. I have met with cases 
in which the roentgenogram showed all the conventional signs of pleural 
adhesions but puncture revealed a free pleura, and complete collapse 
was easily obtained with three or four inflations. More often yet the 
roentgenogram shows a clear picture and it is concluded that the pleura 
is free, but puncture shows conclusively that there are adhesions. One 
sign of freedom from adhesions should be emphasized: I have invari- 
ably been able to introduce gas into a pleura over which friction sounds 
were audible during auscultation. On the other hand, feeble breath 
sounds, or complete absence of breath sounds, is in most cases an 
indication of adhesions. 

Pleural adhesions are almost always present m cases with a history 


804. OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


of pleurisy with effusion in the recent or distant past. Indeed, if during 
the treatment an effusion occurs, its absorption is In most cases followed 
by adhesions, irrespective of the measures we may take to prevent their 
occurrence, and we cannot again induce a pneumothorax when indica- 
tions arise. On the other hand a history of dry pleurisy is no indication 
of pleural adhesions. Many cases remain with free pleural cavities. 

Forlanini is guided by tidal percussion of the margin of the lung, 
especially at the base. When he finds that the base line in the axilla 
shifts between 10 and 12 em. during extreme inspiration, as compared 
with extreme expiration, he is convinced that the pleura is free. Good 
mobility of the lung margins is the most important sign of freedom 
from pleural adhesions, according to Forlanini, but he adds that 
immobility is not a sure sign of such adhesions and of obliteration of 
the pleural cavity. There are cases of extensive hepatization of the 
lung in which the mobility of the lung margin is defective or absent, 
yet the pleural cavity is free. 

It appears that the most reliable means of ascertaining whether or 
not the pleura ws free is the attempt to enter it with the needle connected 
with a manometer. In case the first puncture does not yield negative 
pressure in the manometer—a very frequent occurrence, so that when 
one enters successfully with the first puncture he considers himself 
lucky—another attempt is made at a different point. I have made 
in one case four punctures before succeeding in entering the pleural 
‘avity and in another twelve before giving up the case as not suitable 
for the treatment. Forlanini made fifteen punctures in one case before 
he finally succeeded. It should be mentioned that at times failure to 
find negative pressure is no positive indication of complete obliteration 
of the pleural cavity by adhesions. In one case in which I could not 
enter after trying twice, a spontaneous pneumothorax occurred later. 
Giesemann! reports 3 cases, and Sedlmeyr? 1 case of spontaneous 
pneumothorax after failure to produce one artificially. 

The skin at the site selected for puncture is painted with tincture 
of iodine and the excess is washed away with alcohol. It is then frozen 
with ethyl chloride and an injection of one-third of a grain of novocain 
or cocain in 1 to 2000 adrenalin solution is made. At first the skin is 
infiltrated, then a few drops are injected into the intercostal muscles, 
and finally into the pleura. The latter must not be neglected; it 
appears to be the only known way of preventing pleural shock, of 
which we shall speak later on. 

Thoracocentesis.—The patient is always in the recumbent position 
during the operation, either on an operating table or, preferably, in 
his bed. With a view of widening the intercostal spaces, the hand of 
the side to be operated upon is placed over the head. The selected 
intercostal space is carefully palpated with the index and middle fingers 
of the left hand to make sure of avoiding a rib when thrusting the 





1 Beitr. z. Klin. d. Tuberk., 1918, 33, 215. 
2 Miinchen. med, Wehnschr., 1921, 68, 949, 


TECHNIC 805 


needle into the chest wall. Ifa blunt needle is used, the skin is first 
punctured with a tenotome. The needle is inserted and pushed slowly 
forward, passing through the subcutaneous tissue, fascia, and muscles. 
While the latter are passed the needle goes smoothly, but when the 
endothoracic fascia is reached a certain amount of resistance is en- 
countered, which is characteristic to the experienced hand. Often 
a snapping sound is audible. A similar but stronger resistance is felt 
when the pleura is passed and it is often difficult to decide with confi- 
dence as to whether it was the fascia or pleura which was punctured. 
“Never move the needle sidewise, for if it should be in the lung the 
latter may be easily torn by it.’’ (Balboni.) The manometer is the 
only means at our command to make sure of where the lumen of 
the needle is. 

How far the needle is to be pushed depends on the thickness of the 
chest wall of the given patient. All efforts are to be made to avoid 
penetrating the lung. While in the vast majority of cases this is 
entirely harmless, in rare instances it may prove a serious, and even 
a fatal accident. We may induce a spontaneous pneumothorax, an 
accident which occurs more often than is generally appreciated. 

The usual length of the needle, Floyd’s modification of Brauer’s, 
is5 to 6 em. This is excessive and Saugman’s needle, which is only 
3 cm. long, is at present used by me exclusively. Saugman noted in 
100 cases in which he succeeded in inducing pneumothorax the depth 
to which it was necessary to penetrate the chest wall as far as the 
pleura; and in none of them was it deeper than 3 cm.; in the vast 
majority it was only between 1.5 and 2.5 cm.; in some less than 1.5 
and in one even less than 1 cm. 

Technic of Insufflation.—As soon as the lumen of the needle penetrates 
the costal pleura, and there are no adhesions at the point of penetration, 
the fluid in the closed limb is seen to be sucked up; it rises more or 
less high. In some cases the suction is so pronounced that the fluid 
shoots up to the upper end of the tube and care must be taken that 
it is not aspirated into the pleura. Usually it is elevated between 
1 and 6 cm. and oscillates. The patient is told to take a deep breath, 
and it will be observed that during inspiration the negative pressure 
is more pronounced than during expiration. This oscillation is the 
only reliable indication that the lumen of the needle is in the pleural 
cavity, but at times there are observed slight oscillations when the 
needle reaches the costal pleura before puncturing it, owing to the 
repiratory movements of the lung. But these oscillations rarely 
exceed 1 cm. and must not mislead us. Only when the negative 
pressure exceeds 38 cm. may we venture to let in the gas, and beginners 
should not do vt with less than 5 or 6 em. negative pressure. 

Manometric Hints.—The manometer is to be watched, especially 
during the first operation. The following are useful guides. 

When the Lumen of the Needle is in the Thoracic Wall.—So long as 
it is outside the endothoracic fascia, the manometer rests at zero. 


806 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


When it reaches the endothoracic fascia, feeble oscillations, due to 
respiratory movements of the pleura, may be seen, but they are of 
slight amplitude, between 0 and 3 on each side of the manometer. 
They should not mislead us into the belief that the lumen is in the 
pleural cavity. The fact that there is no negative pressure proves 
this. In very rare instances, while the needle is yet in the chest wall, 
a sudden or slowly rising positive pressure is noted in the manometer. 
It is an indication that the lumen of the needle has entered a large 
bloodvessel, usually the intercostal artery. The needle should then be 
quickly withdrawn and the punctured point compressed with the finger. 
No harm results from it. 

A slight negative pressure during inspiration, becoming less on expira- 
tion, may be produced when the point of the needle is really not in 
the pleural cavity at all, but pushing the parietal pleura before it. 
The indications are clear—the needle is to be pushed ahead guardedly 
until it punctures the parietal pleura. Allowing gas to enter at this 
point may produce subfascial emphysema (see p. 820). 

After the Needle Has Passed the Parietal Pleura. —When there are 
no adhesions there is at once seen negative pressure, 5 to 10 cm., and 
distinct respiratory oscillations, higher on the side of the manometer 
which is connected with the needle than on the side communicating 
with the outer air. If the patient holds his breath during inspiration 
or expiration, or the injection is stopped, the pressure remains negative 
or positive, respectively. 

But at times we meet with this anomalous condition: On passing 
the parietal pleura the fluid in the manometer rises high, showing nega- 
tive pressure of 10 cm. or more, but then it remains stationary. We 
know then that the lumen is in the pleural cavity, and that there are 
no adhesions, but we hesitate to proceed with the injection because 
there are no oscillations. It is clear that the lumen of the needle was 
for a moment between the pleural surfaces, but it has either pushed 
the visceral pleura ahead of it, or entered the lung, or it has become 
clogged. In the former case slight withdrawal of the needle will 
reéstablish oscillations; in the latter case we put the obturator into 
the lumen of the needle and clear it. 

In case there are dense adhesions and the needle does not enter the 
pleural cavity, the manometer stays at zero and does not oscillate; or 
when slight oscillations are noted they are but 1 or 2 cm. and equal 
on both sides, or slightly positive. 

When there are slight and yielding adhesions, there is feeble negative 
pressure, about 2 or 3 cm., and slight oscillations. Occasionally the 
adhesions yield and the negative pressure, as well as the oscillations, 
suddenly increase. But usually the pressure becomes positive soon 
after the introduction of some gas, indicating that a gas pocket has been 
created. During reinflations, sudden drops in the pressure, due to. 
breaking up of adhesions, are more common than during primary 
inflations. 


TECHNIC 807 


When the Lumen of the Needle vs in the Lung.—The manometric 
indications will differ according to the structures the needle has pene- 
trated. If it is in consolidated lung tissue there will be no change in 
the level of the fluid in the manometer; it rests at zero. If the lumen 
is In a bronchus or bronchiole, there is usually no negative pressure, 
but there may be slight oscillations of equal excursions. The amplitude 
of the oscillations will depend upon the character of the respiration, 
whether tranquil or labored. When the patient speaks, the respiratory 
effort with a closed glottis produces, while it continues, a greatly 
increased pressure, greater still on coughing. When the patient holds 
his breath, in inspiration or expiration, the manometric readings are 
again zero. In many cases allowing gas to enter the lung is harmless; 
it passes out through a bronchus. But in rare instances, when the 
lumen of the needle is in the parenchyma, gas may enter the interstitial 
tissues and produce interstitial emphysema (see p. 820). 

If after inserting the needle during the first attempt at inflation 
positive pressure is noted during expiration, it is proof that the lumen 
is in the lung or in a bloodvessel. Occasionally it is found that the gas 
flows in freely, but the pressure in the manometer does not ascend. 
This is an indication that gas is escaping as it enters, which could only 
occur when the needle is in a bronchus and never when it is in the 
pleura. “If the key connecting with the nitrogen is quickly opened 
and immediately closed, allowing only a very minute quantity of 
nitrogen to flow in, the manometer then becomes positive, it is because 
the needle is in the lung.”’ (Balboni.) 

If the lumen of the needle vs in a bloodvessel there are no oscillations, 
but slight positive pressure may be observed; if some blood enters 
the needle, which is the rule, the pressure will be rising. When with- 
drawing the needle it will be found that it contains blood, and the 
patient may have hemoptysis. 

Injection of the Gas.—With the assurance that the needle is in 
the pleural cavity, the tube leading to the gas reservoir is opened 
and nitrogen allowed to flow in by aspiration, or pressure when neces- 
sary. After 100 ce of gas have entered, the manometer is again 
consulted, and if still showing negative pressure, another 100 cc 
are allowed to flow in. It has been my habit never to exceed 300 cc 
during the first operation, although many do not hesitate to introduce 
two and even three times as much, and some even attempt to secure 
complete collapse of the lung during the first operation. Murphy 
advised the introduction of 200 cubic inches (3000 cc) at the first 
operation, while Forlanini after mature experience advised only 
200 to 300 ec. Clinical experience seems to favor smaller quantities 
as safer, and many unpleasant, often dangerous, symptoms are thus 
avoided. To change quickly the relations of the thoracic viscera 
is dangerous, Moreover, when adhesions are present, they may be 
forcibly torn apart and cause trouble. When extensive and dense 
adhesions are present, it is often impossible to introduce more than 


808 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


i00 to 200 ce of gas, and the chances of finally securing a complete 
collapse of the lung are rather slim. 

On the completion of the operation the needle is quickly withdrawn 
and the index finger of the left hand placed over the point of the 
puncture and some pressure applied with a view of preventing subcuta- 
neousemphysema. Finally the small wound is sealed with some cotton 
and collodion and the patient is warned against coughing, which he is 
to avoid as far as is within his control. I find a dose of morphine or 
codein is useful for this purpose. It has been my rule to send the 
patient to bed for twenty-four hours after the first operation, irrespec- 
tive of his general condition. 

Method in Urgent Cases.—In urgent cases, as in copious and uncon- 
trollable pulmonary hemorrhages, and when no apparatus and tank of 
nitrogen are at hand, we may resort to Murphy’s method, which he 
describes as exceedingly simple: “Take an ordinary hypodermic 
needle, rub the sharp point dull on a brick, cover the butt end of the 
needle with cotton, which will serve as a filter of the air that is to enter, 
then insert the needle into the pleura at the point of election for the 
production of a pneumothorax. The skin should have been painted 
with iodine and punctured with a tenotome. The idea is to let the air 
enter the pleural cavity through a needle, the cotton filtering it as it 
enters, thus producing a pneumothorax. The finger placed over the 
butt end of the needle serves as a valve. As the patient inspires the 
finger is lifted off the needle to allow the air to enter, and on expiration 
the opening is closed with the finger. In that manner you can pump 
the pleural cavity full of air to any desired degree of compression. If 
the patient becomes too cyanotic, or if the breathing is embarrassed, 
lift the finger from the needle and allow a little air to escape. The 
procedure is now reversed. Close the end with the finger on inspira- 
tion and remove the finger on expiration, so that air will be pumped 
out instead of in.” 

Technic of Refilling. —The introduction of a few hundred cubic centi- 
meters of nitrogen does not collapse or immobilize the lung. This 
must be accomplished gradually by further inflations. In cases with 
free pleuree this is a simple matter considering that a pocket with gas 
has been already created and the needle can be easily introduced into 
it. For this reason it is best to do the second inflation in the neigh- 
borhood where the first puncture was successfully made, so that it 
enters the gas pocket, and only exceptionally is another place chosen. 
In the latter case we are guided by the same principles as during the 
primary puncture. 

One thing is to be remembered: ‘The manometer is always to be 
consulted before the gas reservoir is opened and, in case no respiratory 
oscillations are seen, the stylet is to be inserted into the needle on the 
assumption that the lumen may be clogged, which is often the case. 
If no oscillations are even then observed, the needle is to be withdrawn 
and reinserted in another place. Accidents have happened during 
later inflations just as during primary operations. 


TECHNIC 809 


The quantity of nitrogen introduced during refills depends on the 
case. My way has been to introduce between 300 and 600 ce at the 
second and 800 to 1200 at the third operation, provided the patient 
bears it well. But when I find embarrassment of the circulation, 
dyspnea, or pain in the chest, I proceed slower and am satisfied with 
300 ee given every other day until complete collapse is attained in two 
or three weeks. We are also to be guided by the final pressure after 
each inflation. In many cases we get positive pressure after several 
hundred cubic centimeters of nitrogen have been introduced, although 
there is no complete collapse of the lung. We often meet with cases 
in which the gas opens but a small pocket in the pleura and when this 
is filled the negative pressure decreases or vanishes. When oscillations 
are good the pressure may be increased guardedly, consulting the 
manometer after each 50 or 100 cc have entered. Saugman, whose 
experience is unexcelled, found that if the gas does not pass with 10 
to 15 em. water pressure the case may be given up, because higher 
pressure will meet with failure. 

At times it is noted that during a refill the pressure suddenly sinks. 
This is an indication that some adhesions have yielded or, which is 
fortunately exceedingly rare, that the lung has ruptured and the gas 
escapes from the pleura into a bronchus. This may occur when the 
nitrogen is introduced under high pressure and the patient coughs 
vigorously. 

My experience coincides with that of Saugman to the effect that it 
is best that, during the first few fillings, the final pressure should not 
exceed ().5 to 2 or 4 cm. of positive manometric pressure. ‘The condi- 
tion of the patient, as well as his reaction during the succeeding few 
days should, however, be our guide. We must always watch whether 
our aim is not attained with a low pressure, and in many cases 0).5 
to 1 em. above zero is sufficient. Forcible inflations involve rapid 
dislocation of the mediastinum and injury to the other lung. We must 
bear in mind that it is not always imperative to compress the lung. 
In most cases affording rest to that organ by immobilization is sufficient 
to give relief, and this can be attained without high intrapleural pres- 
sure. But in case the patient is not improving, his cough, temperature, 
expectoration, etc., are not influenced favorably, the pressure is care- 
fully and guardedly increased. A final pressure of 10 to 15 cm. of 
water is too high, though many authors state that they have resorted 
to it in some cases. Of course, as a rule, the gas is quickly absorbed 
and within a few days the pressure drops so that the embarrassment 
of the respiration and circulation is ameliorated. The great problem 
is presented in cases in which an incomplete pneumothorax has been 
created and the stiff, unyielding walls of cavities, or dense pleural 
adhesions, prevent the compression of the part of the lung which we 
aim to collapse. Saugman and Forlanini have not hesitated to increase 
_the pressure in these cases to 30 and even 40 cm., and they were 
occasionally rewarded by finally attaining a complete pneumothorax. 


810 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


Frequency of Refilling.—After complete collapse of the lung has 
taken place the frequency of the refillings is diminished. In some 
patients the gas is absorbed slower than in others and we are unable 
to say in advance who is likely to need frequent refills and who is likely 
to need infrequent refills. It seems that those walking around absorb 
the gas sooner than those who remain in bed. A healthy pleura 
absorbs more air than one that is inflamed. Primarily the guides 
for the necessity for refills are the general condition of the patient 
and secondarily the findings on physical examination. An elevation 
of temperature, if not due to an impending or actual pleural effusion, 
is often removed by a refill. The same is true of cough and expectora- 
tion. In those who have the lung completely collapsed, there is com- 
plete absence of breath sounds and adventitious sounds; a return of 
these is an indication that refilling is necessary. The fluoroscope is, 
however, the best guide. But I want to repeat that dyspnea and 
tachycardia, which are often caused by excessive pressure in the pleural 
cavity, are to be guarded against. Likewise, excessive pressure in the 
left pleural cavity depresses the diaphragm and may result in gastric 
disturbances, such as anorexia, vomiting, etc., and concomitant poor 
nutrition. 

The volume of the air within the pleura is influenced by the external 
atmospheric pressure, which depends on altitude. When a patient in 
whom a pneumothorax has been induced while he lived at sea level 
moves to a region of 5000 to 6000 feet above the sea level, the volume of 
the air in his chest increases in volume about 15 to 20 per cent, and the 
reverse. ‘To put the matter more concretely: When a patient in 
New York City with a pneumothorax containing about 3000 cc of 
air goes to Denver, Colorado, the volume of the air in the chest will 
increase 15 per cent, or 450 cc. Conversely, when the pneumo- 
thorax was created in Denver and he goes to New York, it will decrease 
450 ce in volume. For this reason, when a patient has been given an 
injection of air which filled his chest while he lived at sea level, he 
should not be sent at once to a high altitude. Conversely, when the 
patient comes from a high altitude to a low one he needs a refill as 
soon as he arrives. 

Symptoms.—The acute and urgent symptoms of spontaneous 
pneumothorax are never seen in the artificially created pneumothorax, 
excepting, of course, when the lung is penetrated and the spontaneous 
variety complicates matters. The pain, dyspnea, cyanosis and col- 
lapse are never encountered. In fact, the majority of patients who 
have overcome the fear for the operation are ready and well able to 
leave their beds immediately after the operation and attend to their 
affairs. The slight difficulty in breathing, seen in some cases at that 
time, is usually objective, the patient protesting that he feels well 
although he evidently suffers from air hunger of some degree. But 
even this disappears within a couple of days, as has already been men- 
tioned. Only in rare instances, when the gas separates adhesions by 


SYMPTOMS 811 


high pressure, does the patient complain of pain in the chest, which 
is, as a rule, trifling. 

In febrile patients the effects of the pneumothorax are usually strik- 
ing, especially when complete collapse of the lung is attained. The 
fever disappears and, in successful cases, does not return unless there 
is some complication. The temperature chart (Fig. 124) distinctly 
shows the effects of collapse on the fever. In some cases it is noted 
that the fever increases 1° to 3° F. for twenty-four hours after each 
insufflation (Fig. 125), Just as is the case with the reaction after an 
injection of tuberculin. This is probably caused by increased toxic 
absorption, owing to the compression of the diseased lung. In case 
an increase in the temperature, lasting several days, is noted during 
the treatment, we may look for some unpleasant complication, espe- 
cially a pleural effusion. When the pneumothorax does not reduce 
the temperature, we may consider the treatment a failure in this 
particular case. With the disappearance of the fever, the nightsweats 
vanish and this gives the patient great relief. 





September, 1914 
8 CUR Ue ae a 


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Fria. 124.—Showing the influence of therapeutic pneumothorax on the temperature. 


The appetite improves in successful cases, and with this the lost 
strength is gradually regained, and the languor, which is such a strong 
clinical feature of the disease, is replaced by a feeling of well-being. 

It is noteworthy that, in spite of the improvement in the general 
condition of the patients, a gain in weight is not a constant phenom- 
enon in artificial pneumothorax. So long as the general condition of 
the patient is good, and the loss in weight inconsiderable, it should not 
trouble us. When, however, the loss of weight is considerable and 
general symptoms, such as fever, sweats, anorexia, etc., make their 
appearance, we may first try to reduce the pressure in the thorax, and 
if this does not ameliorate the condition, the treatment may have to 
be given up. 

Great relief is usually obtained in patients who suffer from severe 
coughing spells which keep them awake during the night. This is 
especially true of unilateral cases in which a large cavity is emptied 


812 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


by compression. After the first three or four inflations it is constantly 
observed that the amount of sputum expectorated is augmented 
because the pressure exerted by the gas empties cavities and bronchi 
of their contents. After the lung has completely collapsed, or the 
cavities have been emptied in partial pneumothorax, the quantity of 
sputum diminishes, and in unilateral cases expectoration ceases 
altogether. In many cases tubercle bacilli are not found in the sputum 
after the lung has been compressed for two months. 

The effect of a therapeutic pneumothorax on the blood picture was 
studied by Gutstein,! who found that in cases of complete and uncom- 
plicated pneumothorax the number of red cells increases rapidly, and 
the percentage of hemoglobin rises slowly. The total number of 
leukocytes decreases, the lymphocytes increase, and eosinophilia 
occurs. When the collapse of the lung is not complete, and when there 
are complications, these blood changes are not constant, and in many 
cases the reverse was observed, a decline in the percentage of hemo- 


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Fie. 125.—Showing the influence of therapeutic pneumothorax on the temperature. 


globin, increase in the number of leukocytes, and a decrease in the 
number of lymphocytes. The blood picture may be used for prog- 
nostic purposes: when it shows improvement, the case is progressing 
favorably, and the reverse. 

More striking than the improvement in the general condition is the 
cessation of hemoptysis when the first inflation is made in a case of 
hemorrhagic phthisis in which the patient is in constant dread lest 
the hemoptysis recur. If we succeed in collapsing the entire lung, 
the hemorrhage ceases at once. The intrapleural pressure acts here 
like a tampon in uterine hemorrhage. But in some cases the area of 
lung tissue containing the bleeding vessel is adherent to the chest 
wall and the intrapleural pressure is powerless to collapse the rigid 
walls of the bleeding cavity. The result is that the bleeding continues. 
On the other hand, in some cases we obtain but partial collapse of 
the lung, but the part containing the bleeding vessel is compressed, 


1 Ztschr. f. Tuberkul., 1916, 26, 336. 


PHYSICAL SIGNS 813 


and the hemorrhage is thus stopped. Hemorrhages may occur in 
patients with pneumothorax. As a rule the blood is derived from 
the untreated lung, but there are exceptions. The uncollapsed cavity 
may bleed. At times an increase in the pressure may help in the 
last class of cases. 

In many, though not in all cases, there occurs some dyspnea during 
the operation or immediately after. But this is, as a rule, transitory. 
In fact, when the dyspnea is due to fever or toxemia it disappears 
after the induction of pneumothorax. If excessive pressure is per- 
mitted to prevail in the treated pleura, dyspnea is likely to occur which 
is usually transitory. The absence of the dyspnea, despite the cutting 
of the breathing area in nearly one-half, is not surprising because, 
in pneumothorax and in pleural effusion, a reduction of 66 per cent 
of the respiratory area does not materially alter pulmonary ventila- 
tion, nor the chemistry of respiration, provided the patient is at rest. 

It appears that a human being can live on much less than two-fifths 
of the normal breathing area in the lungs. Some years ago 8. J. 
Meltzer! called attention to the factors of safety in animal structure 
and economy, to the extravagance of Nature in furnishing most 
of the vital organs with a large surplus of tissue above the amount 
absolutely necessary to perform their physiological functions. Life 
may continue even when the greater part of the lung is destroyed, 
provided the disease which caused the destruction is arrested. We 
see this in cases of pneumonia, pleurisy with effusions, ete. In cases 
of pneumothorax J. H. Means and G. M. Balboni? found that while the 
patient keeps at rest, respiration, gaseous exchange, carbon dioxide 
tension, and the mechanical factors are normal. The ventilation of the 
blood is accomplished almost normally despite the fact that one lung 
is out of commission. It is for this reason that patients with pneumo- 
thorax are dyspneic only on exertion. 

Physical Signs.— Recalling the physical diagnosis of pneumothorax 
as given in text-books, we are surprised that most cases of artificial 
pneumothorax show but few of the supposedly pathognomonic signs. 
Thus, tympany is not a constant sign; in some cases the treated 
side of the thorax is simply hyperresonant and, in contrast with the 
untreated side, only shows a tympanitic overtone, because of the 
vicarious emphysema in the latter, which is hyperresonant or even 
tympanitie on percussion. It is hazardous to diagnose pneumothorax 
on signs obtained by percussion alone. The only feature that may 
give a Clue is displacement of the heart, especially in cases of left-sided 
pneumothorax, in which even a small amount of air may shift this organ 
to the right. 

When there is complete collapse of the lung topographical percus- 
sion will show all the lung margins far out of the normal. r6énig’s 
resonant field of the apex is abnormally wide; the lower margin is 


1 Harvey Lectures for 1906-1907, p. 170. 
2 Jour. Exper. Med., 1916, 24, 671. 


814. OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


low, so that the hepatic dulness in the right side, or the splenic dulness 
in the left, is obliterated. But, what is of more significance, the 
tympanitic sound may be audible far out beyond the sternum on 
the untreated side because of ‘ballooning’’ (see p. 815), and the 
cardiac dulness may also disappear. As was already stated this 
occurs more often in left-sided pneumothorax. In fact, a small 
amount of gas may have this effect in left-sided pneumothorax, and 
may be considered a good sign that the operation was successful. 
In some cases of complete pneumothorax the cardiac dulness dis- 
appears altogether. 

On auscultation, when complete collapse has been attained, we find 
total absence of breath sounds, as well as any adventitious sounds which 
may have been audible before the gas was introduced. In these cases 
we may be guided by the auscultatory findings as to the necessity for 
refillings. When the breath sounds are again audible it means that a 
considerable portion of the air has been absorbed and must be replaced 
at once. Especially is this true when rales reappear in places where 
they were audible before the lung was collapsed. However, we meet 
with cases of good collapse of the lung, but large bronchi remain open, 
and, under circumstances which are as yet not clear, we hear distinct 
and exquisite amphoric breathing; at times even metalic sounds; which 
shows that the teachings of some text-books to the effect that the 
amphoric phenomena in pneumothorax are invariably due to broncho- 
pleural fistule is erroneous. They are evidently due to sounds originat- 
ing in the bronchi which reverberate in the air-filled pleural cavity. 
A metallic tinkle is very frequently heard, especially in cases in which 
bands of adhesions run from the mediastinum to the chest wall. 

When such adhesions are thick there may be no changes in the 
breath sounds at all; they act as good conductors of sounds originat- 
ing in the bronchi. I have recently witnessed while examining a 
patient the following phenomena: Metallic breath sounds and a 
tinkle were distinct. But suddenly the patient went into collapse 
with dyspnea, cyanosis, tachycardia, cold extremities, ete. Coinci- 
dent with the collapse, which was evidently due to the rupture of an 
adhesion, all the sounds in the chest, audible a few minutes before, 
disappeared. Adhesions may serve as conductors of adventitious 
sounds engendered in parts of the lung which are not collapsed, as 
well as from those originating in the opposite lung, as will be shown 
later on. 

The pneumothorax is effective in displacing the mediastinum toward 
the untreated side. In some patients there is a “weak mediastinum,” 
and the result is that the displacement is excessive, and distress of 
variable degree may be manifested, such as pains in the chest, dyspnea, 
insomnia, and at times pseudo-asthmatic attacks. In these cases it 
may be necessary to withdraw some of the gas and thus reduce the 
pleural pressure. High pressure may also result in “ballooning” of 
the pleura toward the untreated side at certain so-called weak spots 


COMPLICATIONS 815 


which have been described by various roentgenologists, and by Stivel- 
man! in this country. The inflated pleura may be seen bulging under 
and beyond the sternum especially between the first and the third ribs. 
There are two weak spots in the mediastinum, one above and anteriorly, 
right under the manubrium and upper part of the gladiolus, the place 
where during embryonal life and infancy the thymus gland is located. 
It extends fon about the first to the third ribs. In adults this place 
is filled with connective tissue, elastic fibers, and remnants of the 
thymus. The second weak spot is found in the lower part of the 
posterior mediastinum, in front of the spine and aorta and behind the 
esophagus and heart. Under normal conditions the right pleura 
extends to the middle line, because the aorta and the esophagus are 
located somewhat to the left and prevent the encroachment of the left 
pleura to the right side. With excessive pressure in a pneumothorax, 
and in some patients with a weak mediastinum even with moderate 
pressure, there occurs ballooning of the pleura at either of these two 
points, at times to an extent as to make it appear almost as if there 
were mediastinal or pleural herniz. Anteriorly the pleura may 
encroach upon the opposite side, under the sternum, and even beyond 
it. Posteriorly ballooning is quite common in right-sided pneumo- 
thorax, while in left-sided pneumothorax it is rare for the above- 
mentioned anatomical reasons. Roentgenograms may show this 
hernia as a bright area with a sharp outline. At times it may be dis- 
covered by percussion by its hyperresonant or tympanitic note at the 
side of the sternum; in rare instances rales which are engendered in it 
are audible near the sternum or the spinal column of the untreated side, 
and they may lead to diagnostic error. At times percussion with a 
coin will bring out an exquisite sound. On the whole, it may be 
said that slight cases are harmless; but when the hernia is extensive it 
may lead to irritative cough, distress under the sternum, and compres- 
sion of the unaffected upper lobe of the lung. Reduction of the 
pressure in the pleura may have to be resorted to for relief. Roentgeno- 
grams of these herniz are shown in Figs. 3 and 4, Plate XX. 

The progress of the pneumothorax can usually be followed by noting 
the increase in the area of the thoracic surface over which there is 
either absence of respiratory sounds or amphoric breathing after each 
filling, until finally the complete lung is collapsed and all breath and 
adventitious sounds disappear. 

Complications.—Not all cases of induced pneumothorax run a 
smooth course during the period of treatment. Complications may 
arise during the operation or Immediately after, and while the patient 
goes around with a collapsed lung. Of the former, collapse, gas 
embolism, pleural shock, or pleural eclampsia, pain in the chest and 
subcutaneous emphysema are worthy of consideration; of the latter 
pleurisy, pleural effusion and rupture of the lung are the most impor- 
tant. 

1 Jour. Am. Med, Assn., 1919, 72, 1445. 


816 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


Accidents during the Operation.—At times, when the needle is 
inserted rather high in the intercostal space, a bloodvessel is injured 
and bleeding results. In most cases it is insignificant, but I have seen 
a hematoma about one inch in diameter result. When there is fluid 
in the pleural cavity such bleeding may turn it sanguineous. We 
have not observed any serious effects from these accidents. 

When the intercostal spaces are narrow, and at times because of 
carelessness, a rib is injured by the needle, the patient complains 
of severe pain, but we have not observed the development of periostitis 
as a result of this accident. Even in cases in which there is pus in the 
pleural cavity, pyopneumothorax, injury to a rib with the needle does 
not produce periostitis, though fistulous tracts result very frequently. 

Penetration of the visceral pleura and perforation of the lung occurs 
very frequently, as is stated elsewhere. It is harmless, as long as the 
puncture occurs into healthy lung tissue. The most that can happen 
is sanguineous expectoration for a few hours. This is true when the 
needle is directed vertically downward and not obliquely. In the 
latter case the lung may be lacerated, not only punctured, and the 
leakage of air into the pleura is so pronounced as to produce complete 
collapse of the lung without any air entering from the gas bottle. 
Even this is harmless, as a rule, as long as the laceration has occurred 
in healthy lung tissue. When the puncture is in diseased lung tissue, 
the result is pyopneumothorax, a grave complication, from which very 
few patients recover. 

Pleural Shock.— Pleural shock may be of various degrees. ‘The mild 
forms manifest merely an increase in the rate of the pulse and respira- 
tion, pallor, dyspnea, ete., which pass within a few minutes or an hour. 
I have met with it several times; in one patient it occurred consecutively 
during the first four inflations and I am inclined to attribute it in a great 
measure to his fear for the operation. In one of my cases the shock 
was quite severe, even alarming, yet it passed away within half an hour. 
Several authors have reported fatal cases. 

The etiology, especially of the fatal cases, is not clear. Forlanini, 
Saugman and others are inclined to attribute it to reflex spasm of the 
cerebral or cardiac bloodvessels. It has been observed that thoraco- 
centesis for any purpose may cause collapse or even death in very rare 
instances. Brauer is inclined to attribute the symptoms of shock to 
gas embolism in most cases and says that the fact that it is usually 
transitory does not exclude gas embolism. But pleural shock may 
occur without any gas inflations. James A. Lyon! mentions a case 
occurring while injecting novocain into the pleura. 

That this accident is comparatively rare is evident from Forlanini’s 
figures to the effect that operating on 134 patients, not including those 
in whom he failed to produce a pneumothorax, and making more than 
10,000 operations, he met with pleural shock only twelve times. 


1 Boston Med. and Surg. Jour., 1914, 171, 329, 


PLATE XXVII 


Fra. 1 





Complete pneumothorax in right pleural 
cavity, but there are several bands of 
adhesions running from the mediastinum 
to the diaphragm. Left lung shows 
moderate peribronchial infiltrations and 
a few calcified glands at the hilus. Lower 
two-thirds markedly emphysematous. 


Inve 3} 








Incomplete pneumothorax in upper 
part of the right pleura. Owing to dense 
adhesions no more gas could be injected 
and the treatment was discontinued. Note 
the stomach at the left diaphragm. 





Fig. 2 





Spontaneous pneumothorax following 
first inflation in an attempt at creating 
an artificial pneumothorax in left pleura. 
Diffuse peribronchial infiltration through- 
out right lung. Heart dropped, slightly 
displaced to the right. Pleuropericardial 
adhesions on left side. 


Hie. 4 





Narrow strip of pneumothorax in right 
pleura along the axillary and diaphragma- 
tic margins. Small amount of fluid in 
costophrenic sinus. Several cavities in 
right lung; one of the cavities contains 
fluid. Apex fixed by adhesions. Left 
lung shows marked tuberculous changes 
in its upper half. Dark area in midclavi- 
cular region represents a calcified lesion. 


PEAT Ex V LT 


Fig. 1 








Complete pneumothorax of the left 
pleura. The right lung shows diminished 
aération owing to fine, nodular infiltra- 
tion and also to engorgement. Medias- 
tinum completely displaced to the right. 


RrGaes 








Darkness of right lung due to intense 
congestion after induction of a pneumo- 
thorax, excepting at the hilus, where it 
is due to enlarged glands and peribron- 
chial infiltrations. One-half of the left 
pleura is filled with air, but the collapse 
of the lung was not effective in compress- 
ing a cavity with thick walls, situated in 
the first and second interspaces. Medias- 
tinuin displaced to the right. 


ithiwee 





Complete pneumothorax of the left 
pleura with displacement of the heart to 
the right. 








Pneumothorax localized in upper and 
lower portions of left lung, but separated 
by pleural adhesions at about the fourth 
rib, where also a cavity with dense walls 
is seen. ‘These adhesions have interfered 
with the success of the pneumothorax. 


COMPLICATIONS 817 


Among more than 3000 inflations made at the Montefiore Hospital we 
observed it but twice to be sufficiently severe to cause some alarm. 

Gas Embolism.—When the manometer is not properly consulted, 
it is said that at times even when the most careful technic is followed, 
gas may enter a bloodvessel and be carried to any part of the body 
and produce an embolism. Usually one of the pulmonary veins 
is entered; it is well known that negative pressure prevails in these 
vessels. Brauer maintains that one of the veins around an infil- 
trated area of lung tissue, or of pleural adhesions, may be penetrated by 
the needle and gas introduced into the circulation. The nitrogen is 
varried into the left heart, then into the aorta, whence it may travel 
into the coronary arteries or the cerebral vessels. Experimental 
researches have not been uniformly confirmatory of this theory, and 
clinically the symptoms of embolism have been observed in some cases 
even when no nitrogen was allowed to enter through the needle— 
merely after introducing the needle. 

Wolff-Eisner,’ while agreeing that in most instances it is due to gas 
embolism, says that there are some in which thrombi are responsible 
for the symptoms observed. They are derived from the vessels around 
or within the pulmonary or pleural lesion, and dislodged by the needle. 
However, it must be emphasized that symptoms of gas embolism are 
not exclusively encountered in the primary operations, but have 
been met with during refills. 

In many cases gas embolism is difficult of diagnosis. The symptoms 
of pleural shock simulate it to a degree as to render the diagnosis doubt- 
ful in many instances. It is, however, to be remembered that pleural 
shock occurs during several operations in a given patient; in some, until 
they become convinced of the harmlessness of the procedure, while 
gas embolism occurs but once, and is rarely repeated. It has been 
stated that in gas embolism there may be found gas bubbles in the 
retinal vessels. But this must be very rare, because in some fatal 
cases of gas embolism the autopsy failed to disclose the gas within the 
bloodvessels. 

The symptoms are collapse, rapid pulse, irregularity of respiration, 
numbness, giddiness, inequality of the pupils, hemiplegia, ete. In 
some rare cases death has occurred without warning. I have been 
fortunate in not having met with a single case of this kind in my 
practice. Of course, prophylaxis is to be the chief aim while operating, 
and one who does not permit the gas to flow into the chest without 
considerable oscillations of the manometric column is hardly likely to 
meet with a case. . Fatal cases have, however, been met by the best 
and most experienced operators. 

The treatment of gas embolism must be prompt and vigorous. 
Cardiac stimulants, camphor in oil hypodermically, digitalis intra- 
venously, oxygen inhalations, and artificial respiration must be given at 


1 Die Prognosenstellung bei der Lungentuberkulose, Berlin, p. 498. 
52 


818 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


once. Jessen advises venesection, and Neumann uses intravenous 
injections of adrenalin. 

Pains.— Pains in the chest are felt by the patient occasionally during 
the operation. At times, while introducing the needle as far as the 
costal pleura, and before penetrating it, exquisite pains are felt which 
promptly disappear as soon as the pleura is punctured. ‘This can be 
prevented by proper anesthesia of the pleura with novocain or cocain. 
Very often after the introduction of the gas, pains are felt in the chest 
for twenty-four hours, due to breaking up of adhesions, especially 
when high pressure is applied. ‘They are not at all unbearable and need 
no treatment. Abdominal pains may result from lowering of the 
diaphragm by the intrapleural gas pressure, but this is also transitory 
and needs no treatment. 

Spontaneous or Pneumogenous Pneumothorax.—Spontaneous pneu- 
mothorax may occur when the needle lacerates the visceral pleura, or 
when a superficial lesion or cavity of the lung breaks through after the 
pleural sheets are separated by the gas. Forlanini met with 9 cases 
of this kind. Floyd! and Webb? mention it. Meyer® mentions a 
case in which it occurred while preparations were being made for the 
induction of an artificial pneumothorax. According to Brauer and 
Spengler a spontaneous, or pneumogenous pneumothorax may occur 
when the needle happens to strike an emphysematous bleb, and they 
mention a case in which an autopsy confirmed this opinion. Wallgren® 
has met with 2 similar cases. Of course, when this complication is 
due to the entry of the needle into a cavity, or a caseating part of the 
lung, perforation of the lung, with its concomitants, is likely to be the 
result. 

According to W. Parry Morgan, “spontaneous” pneumothorax is 
more often produced while inducing an artificial pneumothorax than is 
generally appreciated. This is confirmed by the occasional cases met 
with in which the treatment is abandoned after a futile attempt to 
introduce gas into the pleura, and a collapsed lung is then discovered. 
Again, a roentgenogram of the chest taken after the first operation 
usually shows evidence of more gas in the pleural cavity than has been 
introduced from the reservoir. While it is common experience of those 
using the method that gas can be detected after 200 to 300 cc have 
been introduced, it has been Morgan’s experience that if the visceral 
pleura is not injured the gas cannot be detected until considerably 
more than 300 or 400 cc have been introduced. He concludes that 
when a pneumothorax is visible in the fluoroscope after introducing 
300 or 400 cc of nitrogen, we have justification for the conclusion that 
roentgenographic demonstration of a pneumothorax after the intro- 


1 Boston Med. and Surg. Jour., 1913, 169, 713. 

2 Tr. Nat. Assn. Study and Prevent. of Tuberc., 1914, 10, 101. 
Pularvele. ie bile. 

4 Handb. d. Tuberkulose, 1919, 3, 180. 

5 Beitr. z. Klinik d. Tuberkulose, 1916, 35, 319. 


COMPLICATIONS 819 


duction of such a quantity of gas is achieved only by this being largely 
supplemented by leakage from the lung. 

On the whole, this complication is harmless in most cases. The 
patient becomes dyspneic, cyanosed, and looks pretty bad for several 
hours, a day or two. But then the circulation adapts itself to the 
altered position of the thoracic viscera, and the patient feels quite 
well. We then continue the treatment by refills according to indica- 
tions. In rare instances, when the needle enters a tuberculous cavity 
or a caseating part of the lung, pyopneumothorax is the result. 







LB 45Cla 
jntrathoracica 


‘Pleura pulmorial 


A 5 BO areas: 
4 f Pleura castais 
an an > Hilus 





Fic. 126.—The different forms of interstitial emphysema. (After Brauer.) I. In- 
terstitial emphysema of the pulmonary septa; leads to real mediastinal emphysema. 
IJ. Adhesion emphysema. III. Subfascial emphysema, which may extend to the neck 
and to the opposite side. IV. The most common form, emphysema of the subcutaneous 
and submuscular tissues. 


Emphysema.—The infiltration of gas into the subcutaneous tissue 
of the thoracic wall around the point of puncture is very frequently 
observed, especially in those operated upon by the Brauer method. 
In the vast majority of cases it is due to the high pressure of the gas 
in the pleural cavity, supplemented by cough, and the air works 
its way along the track of the puncture. It is readily recognized by the 
crepitation elicited on palpation, and is of little significance—passing 
away spontaneously within three or four days or at most a week, and 
further inflations are not contraindicated while it is present. It may 


, 


820 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


be prevented by using thin needles, and warning the patient against 
coughing, or administering some sedative like codein immediately 
after the operation. It has occurred in about one-half of my cases 
after the first or second operation and rarely after later inflations. 

Of more serious import is emphysema of the deeper tissues of the 
thorax, which, fortunately, occurs only rarely and may be avoided 
by careful technic. It is usually due to the introduction of air into 
the subpleural tissue before the lumen of the needle has penetrated 
the costal pleura. When gas enters between the pleura and the 
intrathoracic fascia, so-called subfascial emphysema arises. The air 
in this form of extra-pleural emphysema oscillates with the respiratory 
motions of the chest. When the needle reaches that space and the 
operator is under the impression that it is in the pleural cavity and 
permits further entry of air under pressure, the parietal pleura may be 
separated from the chest wall, and air enters between it and the 
intrathoracic fascia and proceeds upward to the neck producing sub- 
cutaneous, or submuscular emphysema. ‘The separation of the parietal 
pleura and the appearance of air in the neck is often accompanied by 
more or less severe pain. It may occur soon after the operation, or 
several hours later. 

Deep emphysema may also be due to leakage from the pleural 
cavity through the wound made by the needle, the gas being pressed 
by the intrapleural pressure or the respiratory movements especially 
during cough, into the extrapleural tissues. Saugman is of the opinion 
that this may even occur without excessive intrapleural pressure, 
although the latter enhances the chances of its occurrence. The gas 
works its way along the path of the vessels to the posterior mediastinum 
and thence along the vessels and trachea up to the neck, where we may 
discover it by the crepitations along its anterior aspect. It is note- 
worthy that it is often felt earlier on the untreated side of the neck, 
which Saugman believes is due to posture. Rarely, the emphysema 
extends along the vessels to the face, shoulder, arm, and forearm. 
I have seen cases in which the abdominal wall and even the scrotum 
were involved. It may be severe enough to cause dysphagia, and 
pain wherever it occurs. But the ultimate outcome is always favor- 
able—it disappears within a few days or a week. It has occurred 
in several of my cases and, barring the little inconvenience it caused 
them, it was of no significance. But Jessen! reported a case in which 
mediastinal emphysema occurred during the first puncture and the 
patient died from asphyxia. Saugman, who had considerable experi- 
ence with deep emphysema, states that in the patients in whom it 
occurs there are but few chances of inducing a complete pneumothorax 
because of the gas leakage. 

In rare cases the needle hits an adhesion, or penetrates the lung, and 
air is thus allowed to enter the pulmonary tissue, resulting in interstitial 


1 Deutsch. med. Wehnschr., 1913, 39, 1245 


COMPLICATIONS 821 


emphysema. Because the air is, in these cases, within the visceral 
pleura it cannot wander up to the neck, as is the case in subfascial 
emphysema. In both cases, however, the air may be responsible for 
a tympanitic note on percussion and mislead into the belief that a 
pneumothorax has been created. 

Pneumoperitoneum, which has been described by several authors, 
I have observed but once. It may occur when the needle is inserted 
along the lower margin of the chest and the diaphragm happens 
to be unduly high, which is not unusual in pulmonary tuberculosis. 
The lumen of the needle may then reach the peritoneum, between the 
diaphragm and the stomach or liver, producing subphrenic pneumo- 
thorax or pneumoperitoneum. It is to be remembered that there 
also the manometer will show negative pressure, oscillating with the 
respiratory movements. It is difficult to distinguish these oscilla- 
tions from those seen when the needle is in the pleural cavity, but 
if it is carefully watched it will be observed that when the needle is 
in the pleural cavity the negative pressure is stronger during inspi- 
ration, and the reverse is true when the lumen of the needle is in 
the peritoneal cavity. In the case that came under my observation, 
the house physician reported to me that in a patient who had adhe- 
sions of the pleura which prevented me from introducing gas, he 
succeeded in getting into his pleural cavity about 1000 cc of air. 
But the patient stated that he had pain in the abdomen, and that he 
felt as if the air had entered his “stomach.” An examination showed 
that the abdomen was blown up, highly tympanitic on percussion, and 
the roentgenogram showed distinctly gas in the peritoneal cavity. He 
made an uneventful recovery, the air being absorbed within a few days. 

Pleurisy.—Dry pleurisy occurs very frequently in patients with 
artificial pneumothorax. In many cases it is followed by effusions, 
but in some it remains dry and the symptoms pass with a few weeks. 
It may follow exposure to cold, or any of the acute inflammatory 
conditions of the nose and throat. Irregular fever and pain in the 
chest are the most common symptoms. Hyperalgesia of the chest 
wall is another very frequent symptom; pain is elicited on pressure 
of the intercostal spaces. Patients who ceased coughing since the 
collapse of the lung begin again to cough spasmodically and painfully, 
while the dyspnea becomes more pronounced. Physical examination 
may not elicit any signs, but in those in whom there is no complete 
collapse of the lung we may hear a friction sound which disappears 
with a change in the position of the patient, or after the pleura is 
refilled with gas. 

Pleural Effusions.—The most frequent and serious complication of 
artificial pneumothorax is pleural effusion in the course of the treat- 
ment. Its frequency varies with the different reports by various 
authors. Some report as high as 70 per cent of cases, while others 
have met with it less frequently. It appears that those who report 
a low percentage of incidence refer to cases which had not been 


822 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


followed to termination. Some are inclined to attribute it to “colds,” 
or to “rheumatism,” etiological factors which are open to question. 
Others have stated that it is usually due to infection during the opera- 
tion, and maintain that when asepsis is rigidly observed effusions are 
rare, which does not hold, because effusions have been met by the 
most careful of operators. Many authors consider the nitrogen as 
a foreign body which irritates the serous surface of the pleura, pre- 
disposing it to disease. It becomes a locus minoris resistentie, and 
inflammation occurs more easily than in ordinary cases of phthisis. 
Klemperer’s! explanation is more plausible: Disease processes 
which reach the surface of the lung and the visceral pleura cause 
adhesions in patients with normally superimposed pleural sheets, but 
in pneumothorax with separated pleural sheets exudative inflammations 
are the result. Rupture of adhesions which lay bare tubercular foci in 
the pleura may also be instrumental in infecting the complete serous 
surface. 

There are observed three main groups of effusions complicating 
therapeutic pneumothorax: 

1. Purely serous with a poor cytology, and hardly ever abundant. 
They are at times not even recognized clinically, and, after remaining 
for a few weeks, they are absorbed without leaving any evident traces 
behind. 

2. Serous effusions with a large number of cells, which have a ten- 
dency to increase in size so as to almost fill the chest. Their symptom- 
atology is clear cut, producing, as they do, high fever lasting for weeks 
and interfering with the successful outcome of the case. In most of 
these effusions large numbers of tubercle bacilli may be found micro- 
scopically, or by inoculation experiments. At times, they become 
purulent. 

3. Effusions due to mixed infection, of exogenous or endogenous origin. 
In the former case the infection is brought about by an unsterilized 
needle, in the latter, by pyogenic bacteria derived from the lung 
coming into the pleura through the injuries produced separating the 
adhesions. Intercurrent respiratory diseases, tonsillitis, bronchitis, 
influenza, etc., may also be held responsible in exceptional cases. 

Brauer and Spengler? maintain that some exudates convey the 
impression of transudates, especially when they appear while the lung 
reéxpands and strong intrapleural negative pressure is induced. 

Symptoms.—In many patients with pneumothorax there occur small 
effusions which give no symptoms. Because of the small amount of 
fluid in the pleura, it is not recognized clinically; neither physical 
examination, nor roentgenography discloses their presence. In some 
patients these effusions are discovered accidentally. In others, there 
is shght fever and discomfort for a few weeks, but then the temperature 
declines and the patient keeps on doing well. There is, however, one 


1 Berl. klin. Wehnschr., 1911, 147, 372. 
2 Handb. d. Tuberkulose, 3, 225. 


COMPLICATIONS 823 


point which may give a clue. Inflammatory conditions of the pleura 
reduce its absorptive powers and refills are not needed as often as when 
the pleura remains normal. If the intrathoracic pressure rises, and 
overinflation cannot be considered a cause, an exudate is usually the 
cause. The fluid in these cases is clear, and is poor in cells, only 
lymphocytes are found in small numbers. 

In others the onset is stormy, with pain in the chest, fever and 
prostration. An examination at this early stage may not disclose any 
signs of an effusion. But it has been my experience that when high, 
continuous, or irregular fever suddenly appears in a patient with an 
artificial pneumothorax who had been doing well before, there is an 
acute pleurisy, and that signs of an effusion will be discovered within 
a few days. It will, however, soon be noted that the intrapleural 
pressure increases. In many cases the fever declines within two or 
three weeks, dropping down to the level at which it was before the 
complication ensued. In some, the fever continues for months, though 
no signs of mixed infection are discovered. In the afebrile stage the 
exudate may remain within the chest for many months; I have seen a 
case in which it remained for over three years. But the patient was 
doing comparatively well, gaining in strength and weight. Micro- 
scopical examination of the exudate shows that the number of lympho- 
cytes is large, though in many polynuclear elements are in abundance. 
If the exudate remains for a long time it may become cloudy a 
greenish in appearance and polynuclear lymphocytes, as well ¢ 
eosinophiles are found microscopically. Even then, there may be no 
other microérganisms than tubercle bacilli in the exudate. In some 
cases, after remaining purely tuberculous for some time, mixed infection 

takes place, and then they belong to the group of septic pleurisies. 
After the acute stage has passed, the patient may feel quite comfortable 
for a long time, though the fluid in his chest remains quite abundant, 
excepting for the dyspnea on exertion and precordial heaviness which 
trouble him. 

The third group consists in septic exudates, which are fortunately not 
common. The onset may be even more stormy than in the preceding 
group. In some, a chill occurs, followed by high fever; 103° to 104° F. 
is not exceptional. The pains in the chest may be severe. For a time 
the fever is continuous, or remittent, but later it becomes hectic, with 
chills and profuse sweating. It is noteworthy that death during the 
first few weeks is rare unless the effusion is due to perforation of the 
lung (see p. 827). Asarule, these patients last for months despite the 
fever and concomitant symptoms. In some, the fever abates, dropping 
to 100° or 101° F. and the patients live for months with pus in the 
pleural cavity. One of my patients lived thus for three years, was quite 
active at his vocation, when the pus began to point on the chest wall. 
An operation gave him relief for another year, when the pus again 
began to point on the chest wall, and he recently was operated upon 
again, but the operation disclosed that there was merely a cold abscess 


824. OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


of the chest wall. In the majority of cases, however, the fever persists, 
tuberculous changes in other organs, notably the larynx, intestines, 
etc., make their appearance, and finally amyloidosis of the visceral 
organs helps in ushering out the patient. It is noteworthy that 
removal of the pus during the acute stage may increase the fever by 
favoring absorption of the toxic products; this may happen even after 
an exploratory puncture. 

The bacteriology of these purulent effusions is that of empyema in 
general. In milder cases pneumococci and other diplococci are found; 
in the severer and toxic types, staphylococci and streptococci and, at 
times, hemolytic forms of these microédrganisms. As is common in 
mixed infections, the tubercle bacilli are outnumbered by the pyogenic 
germs. The cytology is also that of a severe infection—a high count of 
polynuclear lymphocytes, ete. The blood changes are those of pyogenic 
infections. 

Pleurisy with effusion in the untreated side is extremely rare. So 
far only 6 cases have been reported by Als,! Fishberg,? Stivelman,’ 
Reynier and Rossel, and Zemmin® of pleurisy with effusion in the 
untreated side with a hydropneumothorax after artificial collapse of the 
lung. In the case reported by the writer, a hydropneumothorax was 
complicated by an effusion into the left pleura. Both effusions were 
absorbed within three months, and the patient made an uneventful 
recovery. 

Small effusions are often very difficult to diagnosticate, and even 
roentgenography may fail to reveal them; they are especially liable to 
be missed on a plate which was taken with the patient in a reclining 
position, for obvious reasons. In the erect position careful examination 
of the costopleural sinuses will usually reveal them, especially in the 
left pleura, when the patient is bent toward the affected side while 
he is viewed in the fluoroscope. When more or less copious, the usual 
signs of hydropneumothorax, flatness, absence of breath sounds, 
succussion, and a splash are elicited. The flatness elicited on percus- 
sion shifts with the position of the patient. Now and then, exquisite 
metallic sounds, and a metallic tinkle are heard on auscultation. 

[effects of the Pleural Effusion.—The effects of these effusions depend 
on two main factors: Whether they are copious, and whether they 
are septic. Some authors have stated that small serous effusions are 
rather salutary phenomena, and that they may have a good effect on the 
tuberculous process by the antibodies they produce (see p. 515). But 
personal experience has led me to the conviction that all effusions, 
small as well as copious, turn out unfavorable in most cases. Even 
small effusions reduce the absorptive powers of the pleura, and have a 


1 Ztschr. f. Tuberkulose, 1920, 31, 333. 

2 Am. Rev. of Tuberc., 1920, 4, 659. 

3 Am. Jour. Med. Sci., 1921, 162, 270. 

4 Rev. Méd. de la Suisse Romande, 1921, 41, 169. 
5 Beitr. z. Klinik d. Tuberk., 1921, 47, 169. 


COMPLICATIONS 825 


strong tendency to produce adhesions and more or less extensive 
obliteration of the pleural cavity wherever the two inflamed sheets 
meet. The clots which form in these exudates, even in small ones, 
organize and interfere with further inflations of air, and in extreme 
cases, which are not uncommon, the entire pleural cavity is thus 
obliterated. The thickened pleura is often felt by the operator who 
attempts to reinflate the chest as a very perceptible obstruction to the 
entry of the needle. Later, when these adhesions are organized they 
embrace other organs, especially the trachea, mediastinum, and dia- 
phragm pulling them toward the affected side. Lasting for a long 
time they produce secondary shrinkage of the bony thorax, manifesting 
itself as flattening and retraction of the affected side, the ribs approach 
one another, in extreme cases even overlapping one another, the 
shoulder droops, and the spine bends; the scoliosis having a concavity 
toward the side with the pneumothorax. 

Some writers, in this country B. Stivelman,' say that repeated aspira- 
tions of the fluid, especially after watching its effects on the position 
of the mediastinum, and refilling the cavity with air, will prevent 
adhesions. In my experience, when adhesions begin to form, we are 
unable to prevent them from nullifying the good effects of the pneumo- 
thorax by any known means. Sooner or later it becomes more and 
more difficult to refill the pleural cavity with gas, and the treatment 
must be given up. 

Treatment.—So long as there is no high fever, and especially no 
cardiac embarrassment, it is best to leave these effusions alone because 
they keep the lung collapsed, and this is what we aim at with the 
treatment. Acute inflammatory processes of the pleura reduce the 
power of absorption of this membrane, and refills are not needed as 
often as when it remains normal. 

But in some cases in which the fluid in the pleura accumulates rapidly 
and induces dyspnea, cyanosis, etc., or when the fever and prostration 
are marked, it may be necessary to withdraw part of the fiuid and 
replace it with air, leaving the final pressure at 0, or even below. In 
the usual case of this kind it is preferable to withdraw the fluid because 
we may thus reduce the fever, though many writers state that they 
prefer to withdraw the gas in cases of cardiac embarrassment. How- 
ever, it appears that soon after withdrawal the fluid usually reaccumu- 
lates. In some cases I have applied autoserotherapy—withdrawing 
10 ce of fluid and reinjecting it subcutaneously, and am under the 
impression that it enhances absorption. Brauer objects to autosero- 
therapy in these cases on account of the large number of virulent 
tubercle bacilli in the exudate. But I have never observed a tuber- 
culous abscess at the site of the injection of serous fluid. 

These exudates must always be carefully watched. In case they are 
absorbed too rapidly, the lung reéxpands and may form adhesions, 


1 Jour. Am. Med. Assn., 1921, 77, 12. 


826 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


thus preventing its further collapse by gas inflation. I have given a 
fair trial to the various methods of gas replacement which many 
authors have suggested, and found them of questionable value. 
Withdrawing the fluid and injecting gas instead, either in one operation 
or separately, has not given me the results claimed by some writers. 
Inasmuch as the fluid soon reaccumulates, the intrapleural pressure 
increases enormously, and the patient again suffers from cardiac embar- 
rassment. In some cases it is necessary to withdraw fluid or gas soon 
after a replacement operation. The suggestion that watching the 
position of the mediastinum will give a clue as to the indications does 
not hold in most cases. In some it is held by adhesions and even 
high pressure will not move it much; in others, there is a “weak 
mediastinum,” already mentioned, and it moves with the least amount 
of gas or fluid in the pleura. 

It may be stated again that a copious effusion is a serious complica- 
tion of artificial pneumothorax. In a large proportion the treatment 
must be abandoned sooner or later because of adhesions; in many 
complete obliteration of the pleural cavity results. But even then the 
patient may do fairly well because the fibrosis with which this process 
is accompanied extends into the lung and the patient may recover to 
a degree as to be able to pursue some vocation in which muscular 
exertion is not essential. In other words, the case becomes one of 
fibroid phthisis and the prognosis is fairly good. 

With septic effusions things are different. Pyothorax complica- 
ting artificial pneumothorax is a serious complication. Some last for 
a long time, but in most cases the fever, emaciation, etc., are instru- 
mental in dragging the patient down hill and, within a few months, he 
succumbs to exhaustion, amyloid changes in the viscera, extrathoracic 
tuberculous lesions—of the larynx, intestines, etc. The usual surgical 
treatment of pyothorax is, in most cases, powerless to check the pro- 
gress of the disease and most authors prefer repeated aspirations of the 
pus from the chest, according to indications. Now and then we meet 
with a case in which the pus remains in the chest for months, or even 
years, and the patient keeps afebrile. In the septic cases aspiration 
has its drawbacks: Fistulous tracks are often left at the points where 
the needle is inserted to withdraw the pus. Several surgeons, notably 
Sauerbruch,! Spengler, and others, report good results with thoraco- 
plastic operations. But even when one of these surgical operations is 
successful, the patient remains an invalid. Recently I have seen good 
results with the Carrel-Dakin method of irrigating the pleura. 

In rare instances the pus finds its way out through a bronchus and 
the patient drains it out, spitting large amounts of purulent material 
for months, and finally recovers. In these cases we should instruct the 
patient as to the value of posture in facilitating the expectoration of 
the pus from the chest. 


1 Die Chirurgie der Brustorgane, Berlin, 1920. 


COMPLICATIONS S27 


Perforation of the Lung.—We have pointed out elsewhere in this 
book that small cavities in the lung are often located subpleurally, 
and that caseation and softening of the pleura are not exceedingly rare 
in pulmonary tuberculosis. So long as the pleural sheets are in apposi- 
tion, organized adhesions prevent, in most cases, the breaking through 
of these lesions into the pleural cavity. But a pneumothorax, especially 
if the gas in the pleura is not at a high pressure, will favor perforation 
of these lesions with resulting infection of the pleural cavity. 

In others, as I have seen at necropsies, the rupture is due to adhesions 
tugging upon the pleura, especially during cough, overexertion, etc. 
The tear occurs in these cases at the site of the attachment of the 
tense adhesion. In some cases it may be said to be due to direct 
perforation of the visceral pleura with the needle while attempting to 
fill the pleura. This may be prevented by invariably directing the 
needle vertically downward, and not obliquely, so that if the visceral 
pleura is punctured it is not torn. In rare instances perforation occurs 
through a pleura already filled with pus, and may be considered 
empyema necessitatis, the pus breaking through the visceral pleura. 

Perforation of the lung results in an open pyopneumothorax. But 
in the spontaneous open pneumothorax the air in the pleura, as well 
as the elasticity of the lung, are instrumental in closing the opening 
into the parenchyma, asarule. Here, however, the perforation remains 
open indefinitely because of the rigidity of the pleura, as well as of 
the tuberculous changes in the perforated lung. The result is that 
all efforts at clearing the pleural cavity of septic material prove unavail- 
ing; it is reinfected constantly from the lung lesion. Attempts at 
refilling are futile, because the gas escapes through the opening into 
the lung, and the intrapleural pressure is always that of the external air. 

Perforation is not extremely rare, and has occurred in some cases 
in which before the accident the pneumothorax brought excellent 
results. Burnand! reports that among 300 cases of artificial pneumo- 
thorax perforation occurred fourteen times, which was about the 
ratio observed by most authors. 

Perforation of the lung occurs suddenly. The patient, who may 
have been doing well, is suddenly seized with intense pain in the chest; 
the temperature rises and signs of a pleural effusion soon make their 
appearance. I have had a case in which the perforation occurred dur- 
ing a refill and I noted that the intrapleural pressure, as registered by 
the manometer, dropped suddenly. The subsequent course is that of 
an acutely progressive pyopneumothorax. In nearly all cases the rent 
in the visceral pleura remains open indefinitely, and the pleural cavity 
is constantly reinfected from the tuberculous lesion in the lung. In 
many instances the water-whistle sound may be heard owing to the 
air rushing in during each inspiration through a bronchus which 
reaches into the fluid within the pleura. 


1 Ann. de Méd., 1921, 9, 22. 


828 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


Those who do not succumb soon to this accident, remain with a 
chronic pyopneumothorax, but the pus in the chest is drained through 
a fistula communication with a bronchus. Posture influences drainage. 
Now and then drainage is interfered with and the fever rises. Sooner 
or later hectic fever makes its appearance and amyloid changes in 
visceral organs, the liver, kidneys, intestines, ete., give symptoms. 
Death is finally due to exhaustion. 

The treatment is purely symptomatic. Even in the cases in which 
the purulent secretions are well drained through the bronchi, recovery 
is unlikely. The various operative procedures which have been sug- 
gested have proved of no real value, though Spengler reports some 
success attained by repeated aspirations of the fluid and a series of 
plastic operations. Prophylaxis is, however, the only rational thing 
to observe. Proper technic in inducing pneumothorax, especially in 
handling the needle, is of prime importance. Those in whom there is 
but partial collapse of the lung should avoid overexertion, because of 
the danger of tugging of adhesions and tearing the lung. Maintaining 
moderate or high intrapleural pressure is another excellent prophyl- 
actic measure. This can be attained by timely refills. 

Active Lesions in the Untreated Side.—Kxtension of the disease in 
the other lung is perhaps the most disheartening complication during 
the treatment. It has been stated that it may be caused by an attempt 
to collapse the more affected lung too quickly; the purulent matter 
is squeezed out rapidly, and it travels along the bronchi to the other 
side of the chest, producing pus embolisms. It has also been attributed 
to excessive pressure in the pneumothorax. It has occurred in some 
of my cases and in none could I attribute it to these causes. In 
some of my cases there was a hemorrhage from the untreated lung, 
but it soon ceased. The writer has had cases in which one side of 
the chest was treated by a pneumothorax and the lesion was cured, 
but subsequently a new lesion flared up in the opposite lung, which 
was also treated by a pneumothorax. This indicates that the collapse 
and compression of a lung do not necessarily impair its function 
permanently. 

Indications.—Forlanini at first urged that only far advanced cases 
of phthisis for which everything had already been tried, but no relief 
was obtained, should be given artificial pneumothorax. As a conditio 
sine qua non it was insisted upon that the lesion must be strictly 
unilateral, and that any involvement of the other side of the chest 
is a contraindication to the treatment. 

Factors Entering into the Selection of Cases.— The Form and Stage 
of the Disease.—There are numerous cases of phthisis which are doing 
well and recover, with or without any treatment, medicinal, specific, 
climatic, or institutional, and it is, of course, not advisable to subject 
them to the operation with its potential complications. This is 
true of mild incipient cases, and abortive tuberculosis. Fibroid 
phthisis runs an exceedingly chronic course; the pleura is often exten- 


COMPLICATIONS 829 


sively involved, precluding the introduction of gas into the hemi- 
thorax most affected, and cannot be treated by this method. This is 
also true of the most common forms of fibroid phthisis characterized 
by diffuse fibrosis all over both lungs, and it would be sheer folly to 
treat but one side of the chest. On the other hand, in the later stages 
of diffuse fibrosis, when excavations form in one lung, the question of 
pneumothorax is to be considered, provided, of course, that the pleura 
is free from dense and extensive adhesions. 

It is the acute and progressive form of phthisis in which artificial 
pneumothorax finds its best indications and shows the most striking 
therapeutic results. In the group of cases known as galloping con- 
sumption, tn which the patient is carried off within three to six months 
by a rapidly progressing infiltration, caseation and excavation, there 
are many who can be saved by the induction of pneumothorax. It is 
fortunate that dense pleural adhesions are exceptional in these cases, 
and a pneumothorax can easily be induced. The results are often 
astonishing—with the collapse of the lung, the tachycardia, fever, 
nightsweats, cough, expectoration, etc., disappear, and within a few 
weeks the patient is reinvigorated and may continue to gain in weight 
and strength indefinitely. 

It must be stated, however, that the ultimate results are not as 
good in acute as in the chronic cases. Soon after the lung is collapsed 
the results are marvelous—high fever declines, the appetite returns 
and gains in weight are registered. But these results are not lasting. 
Within a few months, owing to some complication, a change takes 
place much quicker than the initial improvement and the progress is 
now downward. ‘The best results are, after all, obtained in chronic 
eases. On this point most authors, notably Forlanini, Brauer, Speng- 
ler, and Dumarest and Murard,! agree. The reasons are obvious. 
The fact that a case pursues a chronic course is an indication that the 
resisting powers are more or less good. In acutely progressing cases 
the local treatment of the lung does not overcome the low resistance, 
and tuberculous lesions of the other lung, or of extrathoracic organs 
appear, nullifying the reparative process in the treated Jung. 

Another group of cases in which artificial pneumothorax renders 
excellent service are those which have recurrent, copious, and uncon- 
trollable hemorrhages. While, when afebrile, the patients are not in 
grave danger, and death due to exsanguination is rare, yet our efforts 
to prevent recurrence of hemorrhage after one has been stopped by 
keeping the patient in bed for several weeks are often futile, and he, 
as well as those around him, are discouraged. I have had some patients 
who had to remain in bed for two or three months with slight, but 
protracted hemorrhages, one following another. With the induction 
of a pneumothorax, provided we succeed in completely collapsing the 
lung, we have an excellent means of controlling the hemorrhage, 


1 La pratique du pneumothorax thérapeutique, Paris, 1919, p. 189, 


830 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


to prevent its recurrence, and, in addition, to give the tuberculous 
focus an opportunity to heal. 

Considering that the hemorrhage is stopped by the mechanical 
effect—by compressing the lung, and thus plugging the bleeding vessel, 
I used to fill the pleural cavity with gas during the first inflation; in one 
case I thus allowed 2000 ce of gas to enter. But further experience 
has taught me that such large quantities are not necessary. In some 
cases the injection of 300 to 500 cc of gas suffices to stop the bleeding, 
and I now am more conservative in this regard. On the next day 
several hundred cubic centimeters of gas are again permitted to enter — 
the pleura, and refills are made according to indications. 

It is obvious that only one lung may be compressed while the 
second must be left to carry on the functions of respiration, and that 
it is useless to combat a lesion in one lung while the disease is smoulder- 
ing, or progressing in the other. For these reasons, it has been found 
advisable to apply pneumothorax only in unilateral cases. But as a 
matter of fact, in more or less advanced phthisis unilateral lesions are 
hardly, if ever, met with. Clinical experience is supported in this 
regard by autopsy findings. Inasmuch as strictly incipient cases are 
not to be treated by this method for reasons already stated, it is evident 
that in nearly all cases in which pneumothorax is indicated there will 
be found signs of involvement of both lungs and we must be satisfied 
with mild or moderate lesions in the untreated side. 

In practice we find that in the vast majority of moderately and 
far advanced cases the lesions are extensive and active in one lung, 
while in the opposite there is limited involvement, or signs of quies- 
cent or healed lesions. Though not strictly unilateral, these cases can 
be successfully treated by pneumothorax, if not prevented by pleural 
adhesions. 

It is interesting that careful clinical and pathological observations 
have shown that only exceptionally is the untreated lung unfavorably 
affected. In spite of the increased functional activity because of the 
vicarious work it is compelled to do, the lung usually remains in the 
same condition as it was before the opposite lung was collapsed. The 
vicarious emphysema which is, as a rule, produced, increases its size, 
and dilates the alveoli and bronchioles, thus permitting as much air 
to be passed through as before, when both lungs were active. It is a 
common observation that active lesions in the untreated lung improve, 
or heal, after a pneumothorax is induced in the more affected side. 
The factors operative in such cases are not well understood. The 
increased blood supply may have something to do with it. The diminu- 
tion in toxic absorption from the ulcerating and excavated lung may 
give the patient a chance to recoup his natural reparative forces, 
unhampered by the toxemia from extensive suppurating areas. How- 
ever, this is not the rule. In some, lesions in the untreated lung flare 
up and extend, as has happened in some of my cases; copious hemoptysis 
even occurred from the untreated lung. 





COMPLICATIONS 831 


Forlanini, Brauer, Spengler, Saugman, Morelli,! and many others 
have argued that all advanced cases should be given an opportunity 
to benefit by artificial pneumothorax. In far-advanced, bilateral, or 
“hopeless” cases one side is, as a rule, extensively involved, while the 
other side shows only limited involvement, though the lesion may be 
evidently active. In such cases it is urged that the more affected side 
should be treated on the principle that there is nothing to lose and 
everything to gain. Forlanini’s experience has taught him that when 
the untreated side has but a limited, even though active focus, the 
chances of success are better than would be expected a priori. When 
both sides are extensively affected the chances of recovery are slim 
indeed, but improvement in the general condition may be anticipated, 
and prolongation of life is not unlikely. At times, Forlanini says, we 
may be astonished that even such patients are cured. In most cases 
the removal or diminution of toxic absorption gives the patient an 
opportunity to muster his natural forces of resistance and comfort, 
often superior to that obtained in operative procedures for incurable 
cancer of the stomach, may be procured. 

There is another important point to be borne in mind: We are not 
always able to ascertain positively whether the lesion in the less 
affected side is active, quiescent, or even healed. Rales and amphoric 
breath sounds heard over a given area of the chest wall are not always 
autochthonous, but may be in fact transmitted by conduction from 
the opposite side, and this is at times very difficult to differentiate, 
as was already mentioned. Indeed, perfect symmetry in location of 
rales, especially on both sides of the spine in the upper part of the chest 
posteriorly, should always excite suspicion that they may be trans- 
mitted, and on the side on which they are weaker it is probably so. 
The best procedure to ascertain such conditions is to auscultate from 
the affected to unaffected side by moving the stethoscope horizontally ; 
if the rales remain the same in number and character, but more or less 
weaker, they are probably transmitted. We know that rales change 
in character in various lesions, and if we find the character 
and number of the rales on both sides remain the same throughout 
several days, it becomes more probable that they are transmitted from 
the sick side to the healthy side. With the collapse of the lung, the 
rales disappear, and those audible in the untreated lung may also dis- 
appear. 

During and after pulmonary hemorrhage also there are often 
heard rales all over the chest which disappear in the unaffected side 
within several days, but when audible they give the impression that 
both lungs are extensively involved. Roentgenography is of little, 
if any, assistance in clearing up many of these cases. 

Some French and Italian authors have suggested “diagnostic 
pneumothorax” in cases in which we are uncertain whether the disease 


1 Pneumothorax Artificial y otras intervenciones en la Tuberculosis, Montevideo, 
1919. 


832. OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


is active in both sides. The more affected pleura is inflated with gas, 
and the opposite lung is watched. In cases in which the physical signs 
of disease are of the transmitted kind, they disappear soon after the 
lung is collapsed. But in case they persist in spite of a complete 
pneumothorax and the genera! condition of the patient is aggravated, 
the pneumothorax is allowed to be absorbed or, in more urgent cases, 
the gas is aspirated and the lung permitted to reéxpand. I have 
repeatedly resorted to this procedure and have, in rare instances, been 
rewarded by improving, or even arresting the progress of the disease 
in a case which appeared hopeless. 

There are some who believe that even incipient cases ought to 
be treated with pneumothorax. Among these may be mentioned 
Murphy,! Lemke, Bullock and Twitchell, Gray,? Forlanini, von 
Adelung, Piéry, and some others. Murphy and Kreuscher say: “Is 
it well to wait until the outlook is so desolate? Is the lung collapse 
such a desperate operation as to be used only as a last resort?”’ With 
this I am not in agreement. If the treatment lasted only a certain 
and limited time, the patient could be informed of the details and 
given the choice. But, inasmuch as we are not in a position to give 
the patient definite information as to the probable duration of the 
treatment, and a large proportion of these cases recover under the 
old and tried methods, we should not subject mild incipient cases 
to the dangers, complications, and duration of pneumothorax. I 
still hold that only progressive or hopeless cases are to be given this 
treatment. 

Contraindications.—To some extent the contraindications have 
already been given while speaking of the indications, but there remain 
yet to be discussed certain conditions which preclude the induction of 
an artificial pneumothorax, mainly those depending on the clinical 
form of the disease, the coexistence of extrathoracic tuberculosis, and 
of other diseases. Because pneumothorax only acts locally on the 
treated lung, acute miliary tuberculosis, in which both lungs are 
usually equally involved, is not suitable for this treatment. Fibroid 
phthisis with extensive pulmonary emphysema is not suitable for this 
mode of treatment, excepting when, in addition to the emphysema, 
there is a localized, suppurating excavation which is the cause of fever, 
sweats, cough, expectoration, etc., undermining the patient. An 
artificial pneumothorax may be applied as a palliative measure. 

The most important forms of extrathoracic tuberculosis which 
complicate phthisis are laryngeal and intestinal involvement. Clinical 
experience has shown that pneumothorax may relieve these complica- 
tions to an amazing extent. It appears that when the tuberculous 
toxemia, due to an active extensive focus in the lung, is removed 
by a pneumothorax, a slight laryngeal lesion often improves, and 
there are even some cases in which complete cure was obtained of 


1 Interstate Med. Jour., 1914, 21, 266. 2 Tllinois Med. Jour., 1913, 24, 201. 


CONTRAINDICATIONS 833 


both the lung condition and the extrathoracic lesions. A. de Gradi,! 
Zink,? von Adelung, and others, have reported such cases, and Forlanini 
speaks of them, though he confesses his inability to explain them. 
On the other hand, Rénon says that he was struck by the frequency 
of grave intestinal lesions found at the autopsies of cases treated by 
pneumothorax. Dumarest and Murard have observed frequently 
that mild intestinal lesions were aggravated soon after the induction 
of pneumothorax. This is in agreement with the writer’s experience. 
Nearly all cases of pneumothorax that died under our observation had 
intestinal lesions. Conceding that the chances of cure are remote, slight 
laryngeal and intestinal complications should not deter us from apply- 
ing pneumothorax if the case is otherwise suitable, on the principle that 
there is nothing to lose and everything to gain. Of course, advanced 
laryngeal lesions, with dysphagia, and intestinal ulceration, peritonitis, 
and amyloid degeneration of the viscera, are distinct contraindications 
to the induction of pneumothorax. 

Diseases of the heart, bloodvessels, and kidneys have been found to 
materially lessen the chances of recovery with an artificial pneumo- 
thorax, and are therefore mentioned as contraindications to the treat- 
ment. ‘They are all accompanied by disturbances of the circulation, 
and the patients do not bear the deprivation of the breathing area of 
a complete lung. Forlanini, however, has found that when compen- 
sation is good, pneumothorax may be induced with some chances of 
success. Some object to the production of a pneumothorax in persons 
over forty years of age. Rautenberg* reports death within two days 
after induction of pneumothorax in two patients over fifty years of 
age, and points out that rigidity of the thorax, pulmonary emphysema, 
etc., which go with advanced age, are distinct contraindications to 
this mode of treatment. 

Diabetes has not been found to interfere with the successful out- 
come of an artificial pneumothorax, and the same is true of preg- 
nancy. ‘There have been reported several cases in which pneumothorax 
was induced in pregnant women who went on to term, were delivered 
of healthy infants, and continued under the treatment. In one of my 

‘ases the woman was six months pregnant when a pneumothorax was 
induced. The effect on the lung was excellent, complete collapse 
was attained and the general symptoms completely disappeared. 
The temperature chart (Fig. 127) shows clearly the effect on the fever, 
but she miscarried four weeks after the first inflation of gas. It is 
noteworthy that the temperature and the general condition of the 
patient were not influenced by the miscarriage. 

Inasmuch as patients with artificial pneumothorax may have to go 
around with collapsed lungs for many years it is interesting that w hen 
affected with some disease requiring surgical intervention they may be 


Gazz. med. ital., 1910, 61, 281. 
Beitr. z. Klinik d. Tuberkulose, 1913, 27, 155. 
Ztschr. f. Tuberkulose, 1920, 32, 1. 


one 


or 
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834 


OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 






























































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DATE 








The patient recovered. 


Fic. 127.—Effects of artificial pneumothorax on the temperature in a phthisical pregnant woman. 


given a general anesthetic. Rey- 
nier! subjected four patients to 
operations for tuberculosis of the 
kidney, intestine, mastoiditis, etc., 
giving them general anesthesia of 
chloroform and ether for as long 
as forty-five minutes. There was 
not observed any excessive dyspnea, 
cyanosis or shock during and after 
the anesthesia, the surgical wounds 
healed uneventfully, and the con- 
dition of the lungs and pleura re- 
mained unaffected by the surgical 
intervention. 

Real? reports the case of a preg- 
nant woman with a narrow pelvis 
and a small dermoid cyst. A 
Cesarean section was performed 
and the living child and the tumor 
were removed. Both the mother 
and the child did well. 

Pleural Adhesions. — These are, 
strictly speaking, not necessarily 
contraindications to the induction 
of a pneumothorax, but they are 
hindrances to its successful accom- 
plishment. In many cases no nitro- 
gen at all can be introduced, because 
of extensive and dense adhesions 
and, after several punctures are 
made, the case is given up as unsuit- 
able for treatment. Frequently an 
area is found which is free and 
some gas is Introduced, but further 
attempts to introduce a sufficient 
quantity to completely collapse 
the lung meet with failure. This 
failure may be of various degrees. 
In some, the pleura is free only 
over a small area and a small pocket 
of gas can be made, while the rest 
of the pleura is adherent. No im- 
provement in the condition can be 


1 Schweitz Rundschau f. Med., 1921, 21, 
hile 

2 Beitr. z. Klinik d. Tuberkulose, 1914, 29, 
349; 1916, 35, 127, 


PROPORTION OF SUITABLE CASES 835 


expected and the treatment must be abandoned. Pleural adhesions 
often interfere with the treatment in a peculiar way. The pleura is 
free all over the chest, except its upper third, over the tuberculous 
lesion, where it is densely adherent. There may be a cavity in that 
location surrounded by stiff walls. The result is that, while we succeed 
in collapsing the lower two-thirds of the lung, the part which is diseased, 
and which we aim mainly at collapsing in order to expel the pus and 
detritus from the purulent cavity, and thus prevent toxic absorption 
and bring about coaptation of its wall with a view of giving them an 
opportunity to cicatrize, cannot be collapsed, and the disease keeps 
on its usual course. This is notably the case with old cavities having 
stiff fibrous walls which refuse to yield to the gas pressure. Many 
failures are due to this condition. Fig. 1, Plate X XII shows a roentgeno- 
gram of such a case. In spite of all efforts to collapse the lung com- 
pletely, the adhesions around the lesion prevented the collapse of the 
diseased part of the lung. 

Jacobaeus! has succeeded in cauterizing such adhesions and thus 
breaking them up permitting the lung to collapse. He uses for this 
purpose the thoracoscope, making but two punctures without produc- 
ing a wide opening in the chest wall. Guided by the thoracoscope he 
locates the adhesions and cauterizes them with the glowing wire. 
His statistics of 37 cases show that in 27 he severed the adhesions so 
that complete collapse of the lung was obtained. From what I have 
seen of this procedure I have not been favorably impressed by it. 
It is not at all the harmless operation which its sponsor claims. A 
patient who is doing well should not be subjected to thoracoscopy. 

At times the pleural adhesions are not very dense; in fact, slight 
adhesions are said to be present in practically all advanced cases of 
phthisis, and an increase in the pressure while introducing the gas 
breaks them up and success is finally attained—the lung is completely 
collapsed. 

Proportion of Cases Suitable for Artificial Pneumothorax.—The pro- 
portion of cases suitable for the treatment is very small indeed. Statis- 
tics of most writers seem to indicate that less than 5 per cent of all cases 
that come under their observation are suitable for this treatment. 
Hardly 2 per cent of the cases that came under my observation during 
the past ten years could be considered suitable for pneumothorax 
treatment. Lemke? appears to be the only author whose clinical 
experience has been to the effect that he has had to abandon the 
operation in but a small proportion of the selected cases because of 
pleural adhesions. Perhaps the reason is that he operated on incipient 
cases. Bernard’ found among 628 patients only 22 in whom he thought 
pneumothorax was indicated, and among these he succeeded only in 


1 Handb. d. Tuberkulose, 1914, 1, 731; Surg. Gynec. and Obst., 1921, 32, 493. 
2 Jour. Am. Med. Assn., 1899, 30, 959, 1023, 1077. 
’ Le pneumothorax artificiel dans le traitement de la tuberculose pulmonaire, Paris, 


1913. 


836 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


6 cases in completely collapsing the lung, in 11 adhesions prevented 
the creation of a complete pneumothorax, and 3 refused to submit to 
the treatment. J. Courmont found among 352 patients only 31 that 
were suitable. Among 110 apparently suitable cases only in 32 per 
cent could Zink produce complete pulmonary collapse, and in 24 per 
cent he failed to enter the pleura altogether because of pleural adhesions. 

Saugman found that in 33 per cent of the selected cases adhesions 
prevented the entry of gas into the pleural cavity. Even with Brauer’s 
method, the proportion of failures exceeds 25 per cent. It must, how- 
ever, be mentioned here that while in most cases complete collapse is 
best, a partial pneumothorax at times serves a good purpose, and 
many writers report excellent results when only creating one or more 
gas pockets in the pleura, and in some of my cases the improvement 
was remarkable under such conditions. Kuthy,! Faginoli, and, in this 
country, von Adelung even practise partial inflation of the two pleuree 
simultaneously in bilateral cases, and they say that the results have thus 
far been apparently beneficial. To my mind this improvement can 
only be seen in chronic cases of phthisis, in which the cavities are 
surrounded by stiff walls of connective tissue, and which do not 
secrete any more. Exquisite amphoric breath sounds are heard over 
such cavities, but no rales. The excavations are not the cause of the 
constitutional symptoms which disable the patient, but the more acute 
patches of infiltration in other parts of the lung are responsible for the 
fever, nightsweats, etc. Compressing these parts we may achieve 
good results. In these cases we hardly ever achieve a cure with 
pneumothorax, because the cavity cannot. cicatrize or contract owing 
to the stiffness of its walls which, together with the pleural adhesions, 
prevents its collapse by the gas pressure. Eut they may be greatly 
relieved by a pneumothorax. However, double pneumothorax is a 
very dangerous affair; I would not venture to induce it. We must 
always bear in mind the possibility of rupture of the lung, or of simple 
spontaneous pneumothorax, which may occur even when the most 
skilled operator is in attendance. In fact, several authors, especially 
Morgan, Faginoli, report rather unfavorable results with this pro- 
cedure. 

Duration of the Treatment.—The question how tong the pneumo- 
thorax must be maintained in order to achieve a cure cannot be 
answered categorically; no rules can be laid down which will apply to 
all cases. In fact, considering that this method of treatment has 
been applied such a short time, there are few who have many cases 
under observation for from six to ten years, and even they have not 
agreed as to the usual duration of treatment of a successful case. 

It appears that we cannot count on less than two years in the most 
favorable cases, although I have had success within one year in several 
cases—the pneumothorax was allowed to be absorbed and _ there 


1 Centralb. f. d. Ges. Tuberkuloseforschung, 1921, 15, 394. 


LIMITATIONS OF PNEUMOTHORAX TREATMENT 837 


occurred no relapse of the disease. But these cases are comparatively 
few. To my mind, the most difficult problem is to determine when 
the healing process has been completed, so that if the lung is permitted 
to reéxpand no active lesion will remain to flare up again by the respira- 
tory movements. This, however, is difficult and, I believe, impossible 
to determine with any precision so long as there is complete collapse 
of the lung, and the general condition of the patient is good because of 
the collapse. Moreover, if we allow the pneumothorax to be absorbed 
too early there may not only be a relapse of the disease, but experience 
has shown that the pleural sheets are likely to adhere, and the fibrous 
bands prevent the formation of a new pneumothorax, if we find that 
this is indicated. 

It is for this reason that whenever we decide to discontinue the treat- 
ment we must watch the patient carefully while the gas is slowly being 
absorbed, and if some symptoms appear, such as fever, cough, expec- 
toration, anorexia, tachycardia, etc., we must at once reinflate the 
pleura. Forlanini says that many patients require a pneumothorax 
indefinitely, which is undoubtedly true, and most authors who have 
had experience with this method of treatment for many years, and had 
opportunities to observe their cases for long periods of time, agree with 
him. 

In his most recent report of 172 cases observed for two to eleven 
years Saugman! says that he thinks “we may consider it a dangerous 
thing to cease treatment before the lapse of more than one year.’’ 
He adds “in chronic cases I am much afraid of discontinuing the treat- 
ment before three or four years, and even after four years relapses are 
not impossible.” He considers the cessation of a pneumothorax always, 
in a measure, a risk, and he lets the patient be treated for about five 
years. But Forlanini, Brauer, and myself have had in some cases good 
and even permanent results after six months’ treatment. Itis, however, 
better to continue for at least two years in all cases. In chronic cases 
we must consider two years as the absolutely shortest period of treat- 
ment, and in doubtful cases it must be prolonged for three and even 
four years. The inconvenience to the patient in having infrequent 
refills, four to six annually, is trifling considering that he can pursue his 
vocation, compared with the hazards of a relapse in case the lung is 
allowed to reéxpand too early. It is therefore better to continue the 
treatment for a year longer than to stop one month too early. If the 
disease is extensive it is advisable that the inflations should be con- 
tinued over long periods of years, perhaps indefinitely. 

Limitations of Pneumothorax Treatment.— We have shown in detail 
the remarkable results of artificial pneumothorax in the treatment of 
tuberculosis, and emphasized the fact that, unlike other modes of 
treatment, this has been applied in advanced and even hopeless cases, 
in cases in which the diagnosis is not in doubt, and which show a ten- 


1 Lancet, 1920, 2, 685. 


838 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


dency to progression. Because of these unquestionable merits some 
authors have pronounced it the most important advance in our attempts 
at curing tuberculous patients. But it has its limitations which should 
be mentioned before dismissing the subject. 

To begin with, very few patients are suitable for the treatment; 
we have shown that the most sanguine find hardly 5 per cent of tuber- 
culous patients can be classed as proper for the treatment, and I am 
inclined to agree with Rénon! that less than 1 per cent of all cases are 
really suitable. In other words, even if all the cases subjected to the 
operation were cured, which is not the case, as we shall soon show, 95 
per cent of the sufferers from this disease would still have to be cared 
for by other methods of treatment. 

The test of a cure should be made on acute and progressive cases and 
here pneumothorax shows that it is very often effective in reducing 
fever, removing symptoms of toxemia, etc. But we have seen that just 
in this class of cases the improvement is not permanent, asarule. After 
an improvement lasting a few weeks or months there is, in most 
instances, a turn to the worse, the patient begins to lose out. In the 
chronic cases many brilliant results are attained. But the majority 
do well for a certain time until some complication compels us to abandon 
the treatment, and the patient must be cared for by the usual methods 
of treatment. In upward of 50 per cent of cases pleurisy complicates 
matters and does harm which is at times actually disheartening. In 
a large proportion, a lesion in the untreated side flares up and we must 
cease refillings. In still others, extrathoracic tuberculous lesions, 
especially of the intestines and larynx, complicate matters, and nullify 
the good effects attained in the treated lung. In a large proportion 
of cases we succeed in compressing the lung excepting the part which 
is the seat of the lesion, and which is held by dense adhesions which 
cannot be separated by gas pressure. In these cases we cannot claim 
success merely because they survived. Nearly all remain with symp- 
toms of chronic phthisis. They survive without pneumothorax in 
many chronic cases. 

Tuberculosis is a very costly disease; when treated with artificial 
pneumothorax it is even costlier. We have shown that the lung must 
be kept compressed at least two years, and in many cases more than 
five. Moreover, while many patients with collapsed lungs are well 
able to work, Rist? even reports the history of a patient with an 
artificial pneumothorax who withstood the hardships of war unscathed, 
the majority are practically invalids as long as they have a collapsed 
lung. The ability to do light work which many writers speak of in 
this connection is not unique to tuberculous patients with collapsed 
lungs. In every hospital for chronic and advanced tuberculous cases 
a large proportion of the patients are fit for light work, and there are 


1 Paris médical, 1921, 11, 24. 
* Presse Médicale, 1914, 22, 692. 


ULTIMATE RESULTS 839 


thousands of persons to be seen in cities who work more or less for 
years despite extensive quiescent lesions in the lungs. 

It is clear that but few patients can raise the funds with which to 
support themselves for years while under treatment. It is decidedly 
wrong to induce a pneumothorax while the patient is in a sanatorium, 
and soon discharge him hoping that he will continue the treatment at 
home. In nearly all such cases that have come under my observation 
the treatment was abandoned soon after the patient left the institution. 
And it cannot be expected under present conditions that sanatoriums 
or hospitals should keep this class of cases for two, three, five, or more 
years. It appears to the writer that pneumothorax treatment can at 
present only be given to the rich or moderately well-to-do who are 
assured of skilful care for a number of years, and have patience to 
continue despite unfavorable complications. 

Ultimate Results.—In the writer’s experience the immediate results 
of the treatment are excellent; in some few cases brilliant. But the 
ultimate results leave much to be desired. It is to be regretted that 
of the thousands of cases that have been treated by this method 
during the past fifteen or twenty years, no properly collated statis- 
tics have been published as to the proportion of patients that have 
completely or partially recovered. The reason is clear when we con- 
sider that it is difficult, if not impossible, to compile statistics of 
results in a disease like tuberculosis which has such a variegated 
symptomatology, and course. The results will always depend on the 
number of acute and progressive cases that are involved, and the num- 
ber of intensely chronic cases that may, and probably would, have done 
well without any treatment. If one institution should care for one or 
two hundred thousand cases, the statistical material would give us a 
fairly good picture of the results of the treatment. But when only 
one or two hundred cases comprise the number reported on, it is clear 
that half a dozen of very acute cases, or of very chronic cases, will 
change the result to an extent as to deceive. In fact, of the various 
reports of ultimate results published, hardly one is satisfactory to a 
trained statistician, and it is a notorious fact that hardly two authors 
have reported comparable material. Lemke hardly ever failed to 
induce a pneumothorax when others, equally competent, fail in 30 to 
40 per cent of selected cases. The reason is, of course, that Lemke 
treated incipient cases, while others treat far advanced cases. Some 
limit their choice to strictly unilateral cases, others treat far advanced 
cases with lesions in both lungs; some avoid acutely progressive cases, 
others give them preference. 

However, we may cite some statistical reports which give some 
idea as to the ultimate results of pneumothorax treatment. The 
most recent is that of Saugman,' who reports on 172 cases observed for 
from two to eleven years, and he compares them with 77 cases in which 


1 Lancet, 1920, 2, 685. 


840 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


he attempted to induce pneumothorax, but failed to collapse the lung 
because of adhesions, ete. He finds that of the 172 cases in which 
he succeeded in collapsing the lung, only 55, or 32 per cent, have 
recovered to a degree that “they are able to do general or light work;”’ 
109, or 63.4 per cent, died from tuberculosis; 3, or 1.7 per cent, died 
from other causes; and 5, or 2.9 per cent, remained unable to work 
because of tuberculous disease. Bearing in mind that 16 of the 55 
classed as able to work were still under treatment when the report was 
published, it is clear that the ultimate results in this series, while 
interesting, is not as brilliant as would appear on superficial examina- 
tion. I have looked over my patients at the Montefiore Hospital 
from this viewpoint and found that of the cases with advanced tubercu- 
losis necessitating hospitalization, 25 per cent could be classed as able 
to do “general or light work,” and they have not been getting any 
special treatment. 

A clearer picture of ultimate results in pneumothorax treatment 
may be gleaned from Dumarest and Murard’s! recent book in which 
there are given figures about 113 cases observed for many years. Of 
these only in 8, or 7.55 per cent, has a complete cure been attained; 
in 7 improvement has occurred, but the lesions are still there, though 
quiescent; in 15, or 14.2 per cent, the lesions remained active, but less 
grave than before the treatment was instituted; in 26, or 24.5 per cent, 
the treatment was still continued when the report was published, but 
the lesions showed improvement; in 9, or 8.45 per cent, the treatment 
was still continued, but the improvement was not striking, and quies- 
cent lesions in the untreated side existed; in 24, or 22.6 per cent, active 
and progressive lesions have developed in the untreated lungs; in 2, 
or 1.9 per cent, the treatment failed because of the poor general condi- 
tion of the patients, and in 3, or 2.8 per cent, extrathoracic tuberculous 
lesions appeared; 8 patients, or 7.55 per cent, died as a result of pleural 
complications, empyema, perforation of the lung, etc.; and 4, or 3.8 
per cent, died because of other complications. 

T'rom these figures it appears that an ideal cure, in which all the 
activity of the disease has been extinguished, the lung permitted to 
reéxpand, tubercle bacilli disappeared from the sputum and the patient 
became able to resume his occupation, was attained only in 8 out of 
113 cases, or in 7.55 per cent. Of the rest, nothing striking has been 
shown. It must always be borne in mind when considering cures in 
tuberculosis, that a large proportion of active tuberculous cases survive 
for many years (see p. 410). Though the average duration of life of 
a person after acquiring tuberculosis is from seven to ten years, those 
with intensely chronic lesions live much longer. And it is in chronic 
cases that the success attained with this mode of treatment is most 
notable. 

For these reasons it is not advisable to apply the treatment indis- 


1 La Pratique du pneumothorax therapeutique, Paris, 1919, pp. 151-159. 


OTHER SURGICAL OPERATIONS FOR PHTHISIS 841 


criminately, but that the cases should be selected with great care. 
I have felt that some cases in which I have applied this mode of treat- 
ment may have done better if they had been cared for in the usual 
manner. Indeed, after mature experience, I have arrived at the con- 
clusion that a pneumothorax should be applied only in cases in which 
everything else has been tried but failed to give relief and there is 
nothing to lose by the procedure; that the potential pleurisies, pyo- 
pneumothorax, rupture of the lung, extrathoracic tuberculous lesions, 
ete., which nullify the good effects of pneumothorax in a large propor- 
tion of cases be all borne in mind, as well as the fact that collapsing 
the lung may prolong life, give comfort and even some efficiency which 
cannot be obtained by any other mode of treatment practised at 
present. Nearly all the present cancer surgery, of which many sur- 
geons speak with justifiable pride, does not give results comparable with 
artificial pneumothorax in hopeless cases of pulmonary tuberculosis. 
No surgeon hesitates in performing the operation of gastrostomy for 
cancer of the esophagus or stomach, knowing that in all probability 
the patient will not survive three months. Palliative enterostomies, 
tracheotomies, etc., are performed with confidence that the best is 
done; even when life is not saved, comparative comfort is given during 
the last days of the unfortunate patient. Likewise, modern radio- 
therapy of cancer gives results which are considered good, the propor- 
tion of permanently cured is surely not higher than that obtained in 
tuberculosis with the aid of pneumothorax. 

In hopeless cases of phthisis pneumothorax does more than the 
palliative surgery and radiotherapy in cancer: It removes or amelio- 
rates the symptoms which make the life of the patient unbearable, 
the cough, the expectoration, the fever, the nightsweats, anorexia, 
hemoptysis, etc.; reinvigorates him and, in many cases, renders him 
efficient at his calling, or even to do some light manual labor, irrespec- 
tive as to whether he is ultimately cured or not. The only incon- 
venience it puts him to is that he must report every month or two for 
a refill, which he knows from personal experience is painless, and 
bearable. In a small proportion of cases artificial pneumothorax is 
even more than palliative; it cures the disease radically and should 
therefore be applied in all cases where other methods of treatment have 
been tried but found wanting. 

Other Surgical Operations for Phthisis.—Extrapleural Pneumolysis; 
Thoracoplasty.— Artificial pneumothorax is not the only method of 
surgical treatment of pulmonary tuberculosis. There have been sug- 
gested operations for the release of the compressed apex of the lung 
by the shortened first rib and ossified cartilage (p. 118); also injections 
of medication right into the lesion in the lung. Th. Tuffier,! in France, 
Sauerbruch,? C. Saugman’ and, in this country, Willy Meyer,! 


1 Paris médicale, 1914, 4, 231; Interstate Med. Jour., 1914, 21, 259. 

2 Die Chirurgie der Brustorgane, Berlin, 1920, contains a thorough study of the subject. 
3 Tubercle, 1920, 1, 305. 

4 Surg., Gynec. and Obstet., 1920, 31, 161. 


842 OPERATIVE TREATMENT—ARTIFICIAL PNEUMOTHORAX 


and Samuel Robinson have developed the operations of eatrapleural 
pneumolysis and thoracoplasty with a view of compressing the affected 
area of the lung or complete collapse of the affected lung. The object 
of extrapleural pneumolysis is practically the same as that of artificial 
pneumothorax, but with this operation only the affected part of the 
lung is compressed while the rest of the parenchyma is left physio- 
logically active. It can be applied in cases in which pneumothorax 
cannot, as when dense adhesions prevent the injection of air or nitrogen 
into the pleura. 

A small piece of rib is resected over the tuberculous lesion, or the 
phthisical cavity which is surrounded by a thick fibrous wall, and an 
adherent pleura which prevents its shrinkage. The lung with both 
sheets of the pleura is then separated from the chest wall between the 
costal pleura and the endothoracic fascia. The lung is then collapsed 
so that the walls of the cavity are brought into apposition. The 
space thus created under the chest wall is filled in with Beck’s bismuth 
paste, bismuth paraffin, or plain paraffin; Tuffier uses adipose tissue, 
fresh or preserved. The wound is then closed properly. No general 
anesthesia is used, because while squeezing out the secretions of the 
pulmonary cavity the lungs may be flooded, and aspiration pneumonia 
may be the result. But local anesthesia is sufficient according to those 
who practise the operation. 

Tufher urges his operation even in incipient cases, saying that we 
should not wait in phthisis till a cavity has formed, any more than we 
wait in tuberculous diseases of joints until suppuration or fistule have 
set in. But the modern treatment of tuberculous joint disease is 
rather conservative, and results are obtained which are superior to 
those obtained with operative treatment. It is doubtful whether the 
operation of extrapleural pneumolysis will ever become as popular as 
that of artificial pneumothorax. 

Thoracoplasty.— Another method of attaining complete collapse of 
the tuberculous lung is the operation of rib mobilization which recently 
has been given preference by thoracic surgeons. ‘To attain collapse 
of the chest wall the operation is usually performed in two stages. 
Some employ a general anesthetic, chloroform being preferred, while 
others use local, or regional anesthesia. A long incision is made 
on the posterior wall of the chest beginning above the first rib and 
extending downward along the outer border of the erector spine 
muscles as far down as the tenth or eleventh rib. Resection of the 
ribs is then done, beginning with the fourth, then the third, second 
and first, followed by removal of the fifth downward. Great skill 
is necessary to remove the second, and especially the first rib. The 
patient is then left for about eight or ten days, when the second 
stage of the operation is done, though in some cases, where the effects 
of the first operation are persistent, it may be necessary to wait 
several weeks before the patient is fit for further operative procedure. 
The aim is to remove the cartilages of the first to the seventh ribs. 


OTHER SURGICAL OPERATIONS FOR PHTHISIS 843 


Surgeons usually begin with the third rib and continue with the second 
and first, then begin again with the fifth and continue resecting the 
sixth, and seventh, while the fourth is left for the end, with a view of 
preventing great collapse before the end of the operation. The details 
of this operation are given in the papers by Meyer, Sauerbruch, and 
others, quoted above and especially in H. Morriston Davies’! book. 
While in the Tuffier operation only partial collapse is attained, rib 
resection gives complete collapse of the chest. 

Phrenikotomie.—Another operation which has been suggested for 
the cure of phthisis is resection of the phrenic nerve with a view of 
procuring rest of the lower part of the lung by paralysis of the dia- 
phragm on the affected side. F. Sauerbruch? and Stuertz have done 
this operation in Europe and Ralph C. Matson and Marr Bisaillon® 
have reported 2 cases in this country. It appears from the few cases 
reported that the operation is of no therapeutic value, if only because 
the diaphragm remains mobile with the respiratory movements after 
the operation. 

More recently Warstat! achieved immobilization of the tuberculous 
lung by excision of the intercostal nerves. He argues that phreni- 
kotomie only immobilizes the diaphragm and restricts the motion of 
the lower lobe of the lung, while the tuberculous process is almost 
invariably in the upper lobe. Cutting the nerve distal from the dorsal 
root from the second to the eleventh, inclusive, he succeeded in immo- 
bilizing the upper lobe of the lung. In animals he found that a few 
weeks or months after the operation the upper part of the lung was 
reduced in size and solid in consistency. In two patients in whom he 
thus operated he noted an unmistakable arrest of the disease. 

These operations, and many more have been suggested and performed 
in isolated cases, may be attractive to the courageous surgeon, but they 
will appeal to the average medical man only in exceptional cases. Very 
few patients will submit to them. ‘To be sure, they are recommended 
only in cases in which all other means have been tried, including 
therapeutic pneumothorax, but no relief has been obtained. But it is 
clear that strictly unilateral lesions are suitable; more so than is the 
case with artificial pneumothorax, which is rather innocuous when 
compared with thoracoplasty. The two successful cases seen by the 
writer have not swayed him in the direction of becoming an ardent 
advocate of surgical interference in pulmonary tuberculosis. ‘The 
results in these cases could be called a surgical success: The patients 
survived the operation. But they remained sick with clinical tuber- 
culosis of the lungs. Numerous patients go around for many years 
with such lesions, coughing, expectorating, and dyspneic without 
having incurred the dangers of this sort of surgery. 


1 Surgery of the Lung and Pleura, London, 1919, p. 212. 

2 Miinchen. med. Wehnschr., 1913, 60, 625. 

3 Tr. Nat. Assn. Study and Prevent. Tuberc., 1915, 11, 183. 
4 Deutsch. Ztschr. f. Chir., 1916, 138, 437. 


CHAP A Th Rosas va 


GENERAL TREATMENT OF THE VARIOUS FORMS 
OF PULMONARY TUBERCULOSIS. 


Incipient Phthisis.—The treatment of the early stage of phthisis, 
immediately after its recognition, varies with the intensity of the 
clinical manifestations of the disease. We have shown that a large 
proportion of cases manifest a strong tendency to spontaneous cure; 
the disease is “aborted”’ within a few months. ‘These patients need 
no treatment beyond stopping work, keeping regular hours, increasing 
the quantity of food ingested, ete. A stay in the country for a month 
or two is even better. In most cases of this type institutional treat- 
ment is not advisable; in fact, I have seen some who were decidedly 
harmed by a stay in a sanatorium, where they were trained into 
carefully studying their disease, and impressed with the dangers of 
slight fever, fatigue, etc. Some have not been as industrious after the 
“cure” as before, though their state of health left little to be desired. 
With workmen having dependent families this is an important point. 

It is different with patients in whom the disease manifests a tendency 
to acute progress; who have fever, nightsweats, cough, anorexia, 
emaciation, etc. These are to be given complete rest of mind and 
body until the acute symptoms are relieved. The best way of attain- 
ing this depends on the financial resources of the patient. The well- 
to-do may be treated at home, or sent to private sanatoriums. The 
results in either case will be the same in the vast majority of cases. 
Under no circumstances, however, should a patient with pyrexia be 
sent to the country, unless he can afford to take along a well-trained 
nurse, and will have competent medical advice. Febrile patients 
who cannot satisfy these two requirements are best treated at home, 
even if the home is only half-way satisfactory. 

The principles of the rest cure, as well as of the treatment of pyrexia, 
have been given in detail elsewhere. Patients who cannot be managed 
at home along these lines should be sent to sanatoriums. 

Patients with limited means should invariably be sent to institu- 
tions for the first few months of the disease, unless they can be moved 
into good homes where they may have appropriate rooms for them- 
selves to carry out the rest and open-air treatment. But after remain- 
ing in the institutions for the period of pyrexia, they may return home 
where they may be cared for just as well as, and at less cost than, in 
the sanatoriums. ‘Those who have no relatives or friends able and 
willing to give them a proper home should remain in the institutions 


ADVANCED PHTHISIS 845 


until the arrest of the disease is assured. As was already stated in 
Chapter XX XIX, the results are the same with home or institutional 
treatment, if the same amount of money is spent upon the patient in 
either case. 

Reasonable patients, running only a subfebrile temperature, may be 
sent to the country for the first few months of the disease. Many 
improve to an astonishing degree, and are cured if the disease is of 
the milder or abortive variety. All patients should be sent out of town, 
preferably to the mountains, if there are no contraindications, for 
the hot summer months. During the winter most phthisical! patients 
do well in the city. 

The dietetics of phthisis have already been detailed in Chapter 
XL. But it should again be emphasized that patients with a 
good appetite and digestion need no special diet, except that they 
should eat more than they had been accustomed to before the onset 
of the disease. In many cases an increase in the quantity of proteins 
and fats is desirable. Those with anorexia and indigestion are to be 
treated for these conditions, because good gastro-intestinal functions 
are the best assets of the phthisical patient. A poor appetite, if not 
improved by open-air treatment, should be stimulated with some of 
the stomachic bitters; creosote in small doses is even better for this 
purpose in many cases. For indigestion appropriate dietetic and 
medicinal treatment is to be instituted. 

In the vast majority of cases medicinal treatment is not necessary 
in incipient phthisis, unless it is for the relief of annoying symptoms. 
Cough may be controlled by the administration of creosote in moderate 
doses. In rare cases sedatives—codein, heroin, dionin, ete.—must be 
given in accordance with the indications discussed in Chapter XLIYV. 
Anemia is to be treated with iron and arsenic. In fact, most patients 
treated at home should be given some medication, even if it is only a 
placebo, and for its psychic effect alone. But there is no doubt that 
ichthyol, creosote and arsenic, given intelligently, exert a good influ- 
ence on the course of the disease. 

The treatment of complications and special symptoms, such as 
hemoptysis, nightsweats, emaciation, etc., has been discussed else- 
where. 

Most patients in the incipient stage of the disease do well under the 
mode of treatment just outlined. Many will recover within a few 
months; in a large proportion the disease will be arrested, but they 
are liable to suffer from relapses sooner or later. In many the dis- 
ease will continue its onward march, irrespective of the treatment 
applied. We then have the so-called advanced stage. 

Advanced Phthisis.—The zeal displayed by medical men during 
recent years to discover and treat early cases has resulted in neglect of 
those in whom the lesion has advanced beyond the stage which by 
common consent is called incipient. Hospital wards for advanced 
phthisis are often attended in a haphazard fashion, and the patients 


846 VARIOUS FORMS OF PULMONARY TUBERCULOSIS 


are discouraged to a pitiable extent. Patients in the advanced stages 
are usually told by their medical advisers to go to some distant climatic 
resort, irrespective of their condition. This is all wrong. There is as 
much hope for the average patient in the moderately advanced stage 
as for a large proportion of incipient patients. Indeed, we have already 
emphasized the fact that the prognosis in advanced phthisis depends 
less on the age and extent of the lesion than on the acuteness and 
activity of the process. 

A patient with an advanced, especially cavitary lesion, owing to 
the fact that he has survived the incipient stage, proves that he has a 
certain but variable amount of inherent resistance against the ravages 
of phthisis. It is our aim to preserve, or rather to increase, this 
power of resistance. This can only be done by proper regulation 
of diet, rest, and exercise, and by avoiding indiscretions which are liable 
to produce acute exacerbations of the tuberculous process. 

We therefore regulate the diet of the patient in such a manner 
that he will not lack in assimilable nourishment (see p. 733). The 
question of rest and exercise is regulated under the guidance of the 
thermometer and the pulse-rate. In hopeful cases all efforts are to 
be directed at avoiding febrile exacerbations, or rendering them short- 
lived if they occur. Many of the afebrile patients may make them- 
selves useful in some direction. Some may even work at their occu- 
pations, provided we find that they are not harmed by activity. The 
fact that one has cavities in his lung, or tubercle bacilli in the sputum 
does not mean that he is disabled. Patients engaged in vocations 
involving no undue muscular exertion may be very efficient. All 
should do something when strong enough to do it, but must cease all 
activities as soon as they feel fatigued, have fever, a rapid pulse, 
dyspnea, ete. This policy has during recent years been adopted in all 
the enlightened institutions for the care of the tuberculous, and the 
patients have benefited much more than by the previous routine rest 
treatment, carried out indiscriminately. 

The diet in advanced phthisis is to be nutritious and of a character 
that will not overtax the digestive organs. At the least indication 
of indigestion, the diet should be appropriately corrected, because, 
next to fev er, indigestion 1s most liable to hurt the patient irreparably. 
Those manifesting a tendency to obesity, and they are not so infre- 
quent as is commonly believed, should restrict the ingestion of fats 
and carbohydrates. A fat consumptive is often more miserable than 
a lean one. 

Medicinal Treatment.—The average patient is not satisfied witb 
hygienic and dietetic treatment, and when no medicinal substances are 
administered he is apt to be led to the belief that there is no remedy 
for him. But there are drugs which have a beneficial influence on the 
course of the disease, as was shown elsewhere (Chapter XLI), and 
medication should be administered. Considering that the patient will 
have to be kept under control for months, it is often difficult to allay 


MEDICINAL TREATMENT 847 


his apprehensions and retain his confidence until the termination of 
the case. It is also a fact, to which we have already alluded, that 
while many remedies have an excellent influence on the disease or the 
patient, they retain their potency for but a short time, asarule. The 
same is true of climatic resorts, and of institutions. The patients gain 
best during the first two or three months’ treatment. 

For these reasons medication must often be changed. Rénon’s 
suggestion may be followed: The patient is given a course of several 
weeks with a certain remedy, and then it is changed for another 
medicament administered for several weeks. The results are often 
remarkable: ‘There are gains in general health, the lesion in the lung 
shows signs of cicatrization, and the patient is encouraged. We may 
thus achieve the same results as with tuberculin without incurring 
the hazards of this dangerous preparation. A good method is to begin 
with ichthyol, administered as directed in Chapter XLI, for four or 
six weeks; or, if the patient thrives on it, it may be continued longer. 
For a week or two it is given in solution; for another fortnight in 
capsules, etc. Then we may give him creosote, or one of its derivatives 
—creosote or guaiacol carbonate, combined with arsenic, for several 
weeks. These substances may be given in mixtures, pills, globules, 
capsules, or by inhalation, as suggested by Beverley Robinson (see p. 
752). Arsenic may be combined with creosote, or given alone in 
the form of Fowler’s solution, or in pill form. Of course, if there is 
a tendency to hemoptysis neither the creosote nor the arsenic is to 
be given. The glycerophosphates are also beneficial, and may be given 
in appropriate doses. They exert an excellent influence on the tuber- 
culous process, promote nutrition, improve the blood picture, ete. 

Medication should be discontinued as soon as there is pyrexia, 
though when the temperature is below 100° F. medication may, and 
should, be given. 

In addition to the above, there is to be given medication according 
to indications as revealed by the symptoms. The anorexia, night- 
sweats, constipation, diarrhea, etc., call for certain medicinal treatment 
which has already been discussed under symptomatic treatment. 

In this manner the average tuberculous patient may get along very 
well for years. Some have very long periods of quiescence, and are 
only rarely laid up with acute exacerbations which need special treat- 
ment, as any acute condition. But they soon recuperate, as a rule, 
and again feel well for a variable period. While many survive acute 
exacerbations occurring at infrequent intervals, provided proper 
treatment is promptly instituted, in most of the chronic cases one of 
these acute exacerbations finally ends fatally. Many succumb to 
intercurrent diseases. ‘These periods of quiescence may be obtained 
by judicious home treatment just as well as by institutional treatment, 
unless we are prepared to keep patients in sanatoriums for many years, 
irrespective of the activity of the disease. And acute and subacute 
exacerbations occur as frequently in sanatoriums and health resorts 


848 VARIOUS FORMS OF PULMONARY TUBERCULOSIS 


as at home, provided, of course, that the patient is well cared for in his 
home. 

Cases manifesting a tendency to progression, with acute or sub- 
acute symptoms and unilateral lesions, should be treated with artificial 
pneumothorax. It offers immediate relief of the symptoms, and shows 
more striking results than any other mode of treatment of active and 
progressive phthisis. Chronic but progressive cases are, at times, 
even more proper subjects for pneumothorax. ‘The indications and 
contraindications are discussed in Chapter XLV. 

Some cases show activity of the process despite the careful treatment. 
All efforts at raising the resisting forces are unavailing, and the disease 
progresses to a more or less speedy termination. All we can do is to’ 
apply symptomatic treatment, and to render the last weeks or days 
bearable and painless. The solacing effects of the derivatives of oprum 
should not be denied these unfortunates. It is, however, one of the 
most common mistakes to send these patients to the country, or 
to sanatoriums. If the patient has a home in which there are no 
infants, he may remain there. If his financial resources are limited, 
the proper place is a hospital for consumptives. We are, at times, 
surprised that under proper care even the most desperate case recu- 
perates, and within a few months returns greatly improved. Rarely, 
they even regain a capacity for working. 

Treatment of Convalescent and Arrested Cases.—A large propor- 
tion of tuberculous patients in the advanced stages of the disease 
improve to an extent as to become useful at their respective occupa- 
tions, although they have not been cured. They cough, expectorate, 
at times the sputum no longer contains any more tubercle bacilli, are 
more or less emaciated, but they have no fever, no tachycardia, etc. 
Physical exploration of the chest shows that there are cavities in 
the lungs, some displacements of the thoracic viscera, etc. Many of 
these are well able to take care of themselves, and even to be efficient 
at some easy occupation. Under proper medical supervision they may 
keep on in this condition for years, even for their natural lives. It is 
very important that these patients have some occupations, otherwise 
they are liable to brood over their condition and become actual hypo- 
chondriaes. ‘The dependent ones are liable to intrench themselves in 
hospitals, and stay there indefinitely; when discharged, they soon seek 
admission to another one. They are very costly to the community, 
as well as to those depending on them. ‘The fact that one has a cavity 
in the lungs or saprophytic tubercle bacilli in the sputum, does not mean 
that he is disabled from working any more than one who has a chronic 
tuberculous fistula or sinus in another part of the body. It is the 
intensity of the constitutional symptoms which should be the guide 
in these matters, and not the findings on physical exploration of the 
chest. 

Once one has suffered from chronic phthisis of some duration, 
he is never cured in the anatomical sense; he is always in danger of 


ACUTE PHTHISIS 849 


a relapse. He should be impressed with the fact that all that was 
attained was an arrest of the process, and that there may be at any 
time a recrudescence of the disease with even greater vigor than the 
former attack. ‘These arrested cases should remain under medical 
supervision for several years, and examined periodically; first fre- 
quently, then at less frequent intervals, so that any tendency to a 
relapse may be checked early by proper treatment. While all efforts 
are to be directed toward prevention of excessive introspection and 
hypochondriasis, yet patients with arrested disease should be instructed 
as to the significance of certain symptoms, such as cough, fever, night- 
sweats, loss of weight, ete: During intercurrent diseases, especially 
catarrhal conditions of the upper respiratory passages and influenza, 
they are to drop all work and take a complete rest. In most cases these 
alleged intercurrent affections are really acute exacerbations of the 
tubérculous process of shorter or longer duration. 

A patient with arrested disease should live in a healthy part of the 
city, in a good home, and sleep in a room with open windows. He 
may engage in his former occupation, excepting the dangerous ones, 
but the workshop must be of the modern and sanitary type, with 
good ventilation, etc. When possible, workmen should become 
gardeners, conductors, watchmen, chauffeurs, letter carriers, etc. 
When feasible, it is advisable that they take up farming. Well-to-do 
patients may move out of the city and settle for life in the country. 
Others may live in the suburbs, or in any country place where they can 
find suitable employment. ‘Those who remain in the city should avoid 
indiscretions. But observing many of this class in the city, I feel that 
those in the country are, in the aggregate, not better off, and have no 
better expectation of life. The questions of marriage, pregnancy, and 
lactation have already been discussed. 

Acute Phthisis.—The acute forms of phthisis are to be treated 
symptomatically, according to indications, so long as we have no 
specific for tuberculosis. In the pulmonary type of acute miliary 
tuberculosis careful hygienic and dietetic treatment is indicated. 
The nursing is of special importance, if we are to make the last days 
of the patient more or less comfortable. The treatment is the same 
as of any other acute or malignant infectious disease. 

Acute pneumonic phthisis is not invariably fatal; often the patient 
passes the acute stage and becomes a chronic consumptive, and the 
treatment is then the same as that given above for chronic phthisis. 

During the acute stage the patient is to be kept in bed, given food 
suitable for a febrile case, and the indications are otherwise met as they 
arise. When the acuteness of the process abates, the patient remaining 
with an active cavity, climatic treatment may be tried. Some of these 
patients do very well when removed from home to some place in the 
country, irrespective of its location or altitude. But they usually need 
a nurse or an attendant. The practice of sending such patients to 
shift for themselves in the country cannot be too severely censured. 

o4 


850 VARIOUS FORMS OF PULMONARY TUBERCULOSIS 


It isfunfortunate that public sanatoriums do not admit this class of 
cases. 

& Fibroid Phthisis.—The patient may feel well and be efficient at 
his occupation for many years, and the treatment at this period is 
purely symptomatic. It is, however, imperative to impress on him 
that overexertion and indiscretions are apt to activate the process. 

Many patients with fibroid phthisis are well nourished during the 
latent or quiescent stage of the disease and need no special dietetic 
instructions. But we often meet with persons suffering from active 
or quiescent fibroid phthisis who are obese. ‘The dyspnea, which is a 
marked symptom in this disease, is more severe in the fat consumptive, 
and it is advisable to arrange the diet so that the patient does not gain 
in weight excessively. Exceptionally, it is even necessary to reduce 
the amount of carbohydrates and fats with a view of reducing the 
weight of the patient. In my experience lean, even emaciated, indi- 
viduals suffering from fibroid phthisis are more comfortable, and live 
longer, than those who are obese. 

In many cases the lodides are very good. ‘The dyspnea is very often 
relieved, expectoration is facilitated, and the general condition of the 
patient improves by the administration for several months of potas- 
sium iodide, or some of the newer albuminate compounds of iodine. 
But this remedy should not be given during febrile attacks, which are 
not frequent in this disease. When fever appears, and is persistent, 
the disease differs but little from common chronic phthisis. Those 
who are subject to hemoptysis, and many fibroid patients suffer from 
recurrent hemoptysis of varying severity, should not be given any 
iodides. It should be discontinued immediately at the appearance of 
streaky sputum. In many cases with profuse expectoration, creosote 
gives relief. 

When signs of asystole make their appearance, with dyspnea, 
edema, ete., rigid rest in bed and appropriate doses of digitalis, stro- 
phanthus, ete., should be administered. 

Fibroid patients should take frequent vacations. The mountains’ 
are not suitable for them because they are more short-winded the 
higher the altitude. It is best to send them to the plains or the sea 
coast. Many do very well indeed in a desert climate, provided they 
can adapt themselves to the surroundings, or “rough it.”’ 

In the later stages, when fever, nightsweats, cough, anorexia, etc., 
ensue, the case is one of advanced chronic phthisis, and is to be treated 
accordingly. 

Pulmonary Tuberculosis in Children.—The acute types of tubercu- 
losis in infants are hopeless, and the treatment is purely symptomatic. 
The infant is to be cared for as a case of pneumonia at that age. The 
only useful thing we can do for infants less than one year old is to 
prevent infection with tubercle bacilli. Once this has occurred, the 
prognosis is very unfavorable. 

We have seen that chronic pulmonary tuberculosis of the type 


PULMONARY TUBERCULOSIS IN CHILDREN 851 


common in adults is practically unknown among children under ten 
years of age. In them the disease manifests itself hematogenously, 
affecting the glands, bones, and joints, and is then the province of 
the surgeon, though it appears from all available data that hygienic 
and dietetic treatment have achieved better results than the knife in 
these cases. The physician encounters in children disease of the 
tracheobronchial glands. Considering that death due to this disease 
is very rare, it is clear that it is bearable by most children. The 
only problem is whether they are all destined to develop phthisis 
when reaching the age of adolescence, or later. This has not yet been 
solved to the satisfaction of all who are entitled to judge. We have 
seen (see p. 584) that when pulmonary tuberculosis does develop in 
one who had extrathoracic lesions during childhood, it is apt to pursue 
a very favorable course. 

The treatment of tracheobronchial adenopathy aims at assisting 
Nature in its efforts to preserve the child. This can best be achieved 
by doing away, as far as possible, with the unnatural method of raising 
children. Growing children should not be kept indoors the greater 
part of the day and night, but should be urged to indulge in outdoor 
exercises and games. Especially is outdoor life imperative when a 
child shows signs of tuberculous infection, or of tracheobronchial 
adenopathy. These children should spend the greater part of the day 
outdoors, and sleep in rooms with open windows. If they can be 
raised in the country it is much better. But in every city, excepting 
the parts known as the “slums,” children may enjoy outdoor life and 
benefit by it. 

It must be borne in mind that children are easily adaptable to life 
in cold air, and most of them can run around the street with scanty 
clothing during very cold days and derive great benefit. They may 
also be given cold spongings followed by friction with a rough towel 
every morning, and thus “hardened.” Only in this manner can 
“colds” be prevented in children. Harmless in themselves, colds 
may, in children with tuberculous glands in the chest, activate the 
tuberculous process and favor an acute exacerbation of the dormant 
tuberculous lesion. However, there are children who do not bear 
“hardening” well. If it is found that these cold spongings and rub- 
bings are not followed by a proper reaction, or that they develop catar- 
rhal conditions of the nose and throat, hardening should be given up. 
Many children are constitutionally unfit for cold baths, and they may 
be harmed by attempts to adapt them to these ablutions. 

The ideal treatment of tuberculous children is to raise them all in 
the country. But like all ideals, it is only attainable by the favored 
few. The vast majority of infected children have to be raised in 
cities, for obvious reasons. But society, which is largely responsible 
for the conditions favoring tuberculous infection, can do a great deal 
toward saving these children, and raising them toward healthy man- 
hood and womanhood, by providing vacations for them once or twice 


852 VARIOUS FORMS OF PULMONARY TUBERCULOSIS 


annually, so that they may recuperate their vanishing forces and 
acquire resistance against the extension of the tuberculous process. 
In New York City this is done for a limited number of children derived 
from tuberculous stock by the Preventorium. In other cities in this 
country similar efforts have been made. But not all that need these 
vacations, proper food, and exercises are accommodated in any city. 

If the parents of a child with tracheobronchial adenopathy can 
afford it they should move to the country, or to a suburb. In some 
cases it is feasible to send the child to be raised outside of the city lines. 
Many authorities maintain that it is best to raise these little patients 
in the mountains, or that they should be sent for frequent vacations 
to a high altitude. But I have seen excellent results in many cases 
which were sent to the seacoast, or to some forest climate. It is 
remarkable how quickly these children recuperate after a few weeks 
out in the open air, away from the city. 

Many of these children do not eat enough, and the emaciation result- 
ing from the smouldering tuberculous process in the chest is increased 
by the lack of nourishment. The anorexia is very often relieved by 
open-air life. A child in the city may not eat enough, or may have an 
actual abhorrence for food. But as soon as it is removed to the 
country, the desire for food is increased; often the appetite becomes 
ravenous a few days after arrival in the country. 

In those who cannot afford to go to the country the anorexia may be 
relieved by open-air life in the city. They should be urged to spend 
the greater part of the day outdoors, and sleep in rooms with open 
windows. In urgent cases there should be no schooling. The modern 
open-air schools are of questionable utility, especially during the 
winter when the bitter cold is apt to prove unbearable to both the 
teachers and the pupils. The child needs not only fresh air, but exer- 
cise is Just as important. This keeps the child warm in the coldest 
day. Ihave very little confidence in the educational value of the open- 
air classes; so far as I have observed, there is hardly any study during 
cold days. <A child run down to such an extent as to need open-air 
life throughout the day and night is unfit for schooling, and should be 
taken out to the country for a few months or a season, or taken out of 
school for a similar period, until it recuperates, when it may resume 
studies. 

The food of these children need not differ from that suitable for 
any child of the same age, but it should be plentiful, appetizing, and 
nourishing. It is even more difficult to place a child on a special diet 
than an adult. And there is no special need for such a procedure. It 
is, however, important to see to it that it does consume a sufficient 
quantity of proteins and fats. In children between two and four years 
of age, milk, cream, and eggs supply these requirements ideally. But 
older children should be urged to eat meats and poultry, and butter 
is the best source of fat for them. It is the most assimilable form of 
fat that can be given to the vast majority of children. Those who do 
not thrive on this diet, or who will not take a sufficient amount of 


PULMONARY TUBERCULOSIS IN CHILDREN 853 


butter, should be given cod-liver oil. The vast majority of children 
take it pure, or with malt. Most of the emulsions contain very little 
of the oil, and are nauseous. 

Children with enlarged bronchial glands will almost invariably do 
well under this mode of treatment. It is often astonishing to watch 
the recuperation of an emaciated child within one or two months after 
being placed under this treatment. It is encouraging to watch the 
great improvement shown by most of the children taken from the 
tenements of New York City to the country. In some obstinate cases 
it is necessary to repeat the vacation twice annually for several years. 
Some should be kept out of town until they reach adolescence. But 
it should always be remembered that they all do well if properly treated ; 
the development of chronic phthisis before the age of ten is exceedingly 
rare, and infrequent before the age of fifteen. 

There is, however, one danger to which these children are exposed. 
The endemic diseases of childhood, measles, whooping-cough, scarlet 
fever, etc., produce anergy or lowered reactive powers (see p. 127) 
to tuberculosis. They are therefore to be guarded against these 
diseases. Many a child, doing well despite tracheobronchial adenitis, 
succumbs to bronchopneumonia complicating measles or whooping- 
cough. It is very difficult to carry out prophylaxis against these 
endemic diseases in children living in the tenements of large cities; 
and in those who attend school in any part of a city, where there are 
so many “carriers.” And we cannot isolate a child from intercourse 
with other children for obvious reasons. This is a fact which is often 
not considered in this connection by those eager to do something 
along these lines. If all efforts at prevention of complicating diseases 
have failed, and the child does develop one of them, the treatment 
should be very careful, and during convalescence the patient should 
be sent to the country for a month or more. 

But infants can be shielded against infection with measles, whooping- 
cough, etc., because they are always in the immediate care of the 
mother. Infants known to have been infected with tuberculosis should 
be kept away from the proximity of other children who are liable to 
be “carriers.” It is during infancy that measles and whooping- 
cough are likely to do most harm when attacking a subject harboring 
tuberculous infection. 

Medical treatment is not indicated in most cases, excepting where 
there is anemia, cough, etc. These symptoms are best relieved by the 
open-air treatment. But we may in many cases assist or accelerate 
the improvement by the administration of iron. The old syrupus ferri 
iodidi may be given in doses of 3 to 5 drops to children three years of 
age, and more in proportion to older children. Iron tropon is another 
good and palatable preparation for these anemic children. 

Children showing catarrhal symptoms, when not due to inflam- 
matory conditions of the nose and throat, do well with creosote in small 
doses. It may be given in doses from } to 4 drop diluted in milk. 
Any of the derivatives of creosote may be given in powder or in syrup 


854 VARIOUS FORMS OF PULMONARY TUBERCULOSIS 


form. This will often relieve a cough much more effectively than 
sedative drugs. 

Specific treatment has been used with less success in children than 
in adults. It must be remembered that statistics of a number of 
children treated with any method, including tuberculin, are of no 
value if they show that of so many treated no deaths have occurred. 
Death due to tuberculosis, excepting meningitis, in children over 
two and under fourteen years of age, is exceedingly rare. For these 
reasons, orphan asylums show such splendid results—children of 
tuberculous parentage do not develop phthisis while they are in the 
institutions. But in children tuberculin is not indicated because the 
psychic effect, which is the main curative factor in adults, is lacking. 
I can see no reason for giving tuberculin to children. 

Tuberculosis in the Aged.—Most aged phthisical patients are 
emaciated and debilitated. In many nourishment cannot be given 
in plentiful amount because they lack teeth for mastication, and most 
of them suffer from disturbances in the motility and secretions of 
the stomach and intestines. They also have arteriosclerosis, sclerotic 
kidneys, and do not bear the ingestion of large quantities of proteins. 
Fats are apt to induce diarrhea more often than in youthful subjects. 

These difficulties in the dietetics of aged consumptives may be 
overcome within limits by first ordering the repair of the teeth. Then 
they may have a diet consisting mainly of milk, cream, and cereals. 
Fish is also well assimilated by aged persons, and they should take it 
when, for any reason, meats are not tolerated. But so long as the 
condition of the kidneys is not such as to contraindicate meats or 
poultry, they may be allowed in moderate quantities. Vegetables 
maly be given so long as there is no diarrhea. While in younger phthisi- 
cal patients alcohol is to be tabooed, it is different with aged patients. 
If they have been accustomed to alcohol it is not advisable to attempt 
instituting reforms at an advanced age. In some cases alcohol is even 
of distinct benefit, if not abused. 

Old patients do not bear outdoor life as well as younger ones. ‘The 
same is true of high altitude. They must have warm rooms for living 
and sleeping. In fact, if they can afford it they should spend the 
winter in some southern region. The intense cold of the winter has 
a very deleterious effect on them because of the defective circulation— 
especially the peripheral—rigid arteries, sclerotic kidneys, pulmonary 
emphysema, ete., with which many are affected. But they need 
fresh air. While they should sleep in warm rooms, the windows must 
be kept open. 

Cardiac derangements are to be carefully treated by rest, digitalis, 
strophanthus, ete. Myocarditis is, however, not relieved by these 
remedies and, in addition to rest, small doses of nitroglycerin, fre- 
quently repeated, often have a beneficial influence. The iodides are 
very good in many cases, and should be given in moderate doses. In 
many patients the dyspnea is relieved by this remedy much more 
effectively and lastingly than by anything else. 





TUBERCULOSIS DURING THE MENOPAUSE 855 


Fever is to be treated according to the principles discussed in 
Chapter XLIII. Most senile patients have no fever, but at times 
we encounter some with pyrexia of longer or shorter duration. Those 
in whom the fever is mild and evanescent require rest in bed until the 
temperature comes down to normal. Very old persons, over sixty 
years of age, do not bear fever very w ell, and must be given anti- 
pyretic treatment. Pyramidon in 5-grain doses may be nmniseered 
three or four times a day. 

The cough and expectoration need no treatment as long as they 
are not excessive. Otherwise, small doses of codein or heroin should 
be given. In many cases the expectoration is profuse and contains 
numerous tubercle bacilli. It may be greatly influenced by posture, 
as in bronchiectasis, and postural treatment may be attempted. 
But this is difficult with old persons, because of their weakness and 
debility they cannot withstand the vigorous cough this mode of 
treatment is apt to induce. 

Tuberculosis during the Menopause.—Tuberculosis in women 
during the menopause is apt to be complicated by symptoms which 
are not seen in other phthisical patients. Considering the profound 
impression made by the tuberculous toxemia on the sexual sphere 
(see p. 610), there is no wonder that at the “critical period” tubercu- 
lous women should present special symptoms. 

Many are more or less obese despite the continued activity of the 
tuberculous process in the lung. Dyspnea is very frequent, and many 
complain of cardiac palpitation. Hemoptysis is very frequent, and 
may replace the menstrual flow, though I should hesitate before 
considering it vicarious menstruation. Copious hemorrhages are 
uncommon; I am under the impression that they are less common 
than among others with similar lesions. But streaky sputum and 
small hemorrhages are very frequent. In addition there are most of 
the usual symptoms of the menopause—hot flushes, headaches, etc., 
and profuse perspiration. Combined with the symptoms of phthisis 
these symptoms of the menopause make this class of patients proper 
subjects for special treatment. 

In addition to the treatment of phthisis outlined above, the special 
symptoms need attention. I have had several cases in which repeated 
hemoptysis was stopped by the administration of the extract of the 
ovaries or the corpus luteum. Indeed, most of the annoying symptoms 
which torture the unfortunate woman more than those caused by the 
tuberculous process, may be relieved by the timely and proper adminis- 
tration of these remedies. It is also a fact worthy of remembering 
that during the climacteric phthisical women do not bear the adminis- 
tration of tuberculin very well; most are apt to be harmed by specific 
treatment. 

The cough and insomnia also are best relieved by the ovarian sub- 
stance; sedatives and hypnotics often aggravate this condition, though 
in many cases bromides and valerianates are effective. 


HUA te ede 
TREATMENT OF COMPLICATIONS. 


Pleurisy.—Dry localized pleurisy occurring during the course of 
phthisis needs no special treatment, excepting to relieve the pain which 
is at times annoying. In mild cases external applications may suffice 
to give the patient comfort. Any of the belladonna plasters, or a sin- 
apism may do; while some apply tincture of iodine. The writer finds, 
however, that the administration of salicylates often relieves these 
pleural pains much better than anything else. Aspirin, in doses of 
from 5 to 10 grains three or four times a day, may be given in cases in 
which sodium salicylate is lable to derange the stomach. 

In acute cases of pleurisy the pain may be very severe during the 
first few days before the effusion appears and may necessitate the 
administration of morphine, } to } grain hypodermically. In most 
cases It is not necessary to repeat it, but it is better to strap the chest 
with adhesive plaster. In plethoric individuals, the application of 
several leeches to the painful area often relieves the pain when every- 
thing else has failed. As soon as the effusion appears the acute pain 
usually ceases. Cetrangolo! suggests the induction of an artificial 
pneumothorax for the relief of pain in acute pleurisy. He found that 
the insufflation of 100 ce of air into the pleural cavity increases the 
pain, but within twenty-four hours it disappears permanently. The 
cases in which this is indicated are rare. 

The patient is to be kept in bed as long as the fever lasts. But 
during the later stages he may be permitted to take mild exercises. 
The diet is to be given in accordance with the temperature and the 
tuberculous process in the lungs. 

It is not advisable to make any efforts to hasten absorption of the 
fluid in cases of tuberculosis. The fluid may be serving a useful pur- 
pose by compressing the lung and facilitating the healing of the lesion 
in the same manner as an artificial pneumothorax does, and also 
because of some biochemical effects (see p. 516). On this principle 
effusions may be permitted to remain for months. But in case the 
effusion causes cardiac embarrassment, severe dyspnea, cyanosis, 
insomnia, and other urgent symptoms, it should be aspirated at least 
partially. But even then aspiration should be left as a last resort, 
because speedy withdrawal of the fluid, and rapid expansion of the 
lung may awaken the tuberculous process in the parenchyma into 


1 Semana Med., 1919, 26, 161. 


EMPYEMA 857 


acute activity. The writer has observed this to happen in several 
cases. 

It is best to first try autoserotherapy. Five to 10 cc of the fluid are 
withdrawn with an aspirating syringe and reinjected into the subcuta- 
neous tissue. A good way is not to remove the needle after the syringe 
is filled with the fluid, but while withdrawing it, when its point reaches 
the subcutaneous tissue, to turn it parallel to the surface of the chest 
and to inject the fluid right then and there, as was described by the 
writer! elsewhere. ‘This can be done several times on alternate days. 
In most cases there will be noted an increase in diuresis, and the level 
of the fluid begins to sink, so that within a couple of weeks it may be 
absorbed altogether. 

In cases in which autoserotherapy is of no avail, and the general con- 
dition of the patient demands removal of the effusion, aspiration should 
be done. It is advisable not to remove all the fluid at one sitting, but 
to do it on alternate days, each time withdrawing a part. In many 
cases the pleura refills soon after tapping, and it is necessary to assist 
the absorption by giving a salt-free diet, and to reduce the amount 
of fluid ingested by the patient. Diuretin may be of assistance by 
increasing diuresis. But other drugs, reputed as assisting absorp- 
tion of pleural effusions, as the iodides, are impotent in this regard. 
Emptying the bowels daily with salines, if there are no contraindica- 
tions, may assist in the absorption of the fluid. 

Many authors treat pleurisies by withdrawing the exudate and 
replacing it with air, claiming that in this manner reaccumulation 
of fluid is prevented. But we have seen that while troublesome, the 
presence of fluid in the chest is not dangerous per se. It is only the 
tuberculous process in the parenchyma of the lung that is dangerous. 
And this is as well controlled by the fluid as by air in the pleural cavity. 
Moreover, converting the pleurisy into a pneumothorax does not 
prevent the reaccumulation of fluid, as experience has taught the 
writer. ‘This is natural when we consider the frequency of exudates 
in pneumothorax. It is also to be borne in mind that a hydropneu- 
mothorax may become purulent, and then the prognosis is very serious. 

Empyema.—The treatment of purulent effusions, during the course 
of phthisis is very unsatisfactory. Some authors have stated that 
when the pus shows diplococci, especially pneumococci, and also 
streptococci and staphylococci, the prognosis is better, and resection 
of one or two ribs may bring about a cure, while in cases in which the 
pus shows the presence of tubercle bacilli, operation is futile. In the 
experience of the writer there has been observed no difference from this 
viewpoint. In very rare instances we meet with a case in which several 
aspirations of the pus cure the empyema. Similarly the writer has had 
cases of localized and encapsulated empyemata which broke through 
bronchi, the pus was expectorated and the patients recovered. In 


1 Jour. Am. Med. Assn., 1913, 60, 962. 


858 TREATMENT OF COMPLICATIONS 


the vast majority of cases we keep on withdrawing larger or smaller 
quantities of pus, but the chest fills up again ina short time. In some 
cases fistule form along the track of the needle, discharging pus 
externally. 

The results of operations for empyema complicating phthisis are 
unsatisfactory. A simple incision for the evacuation of the pus is 
nearly always followed by a fistula necessitating the patient to go 
around with a foul-smelling bandage for the rest of his life. For this 
reason most physicians are at present satisfied with the aspiration 
of the pus, repeated according to indications. Recently I have seen 
excellent results with the Carrel-Dakin method of treatment, and now 
urge it in all cases of pyothorax complicating tuberculosis. 

‘Witenes treated by aspiration or thoracocentesis, the fever usually 
keeps up, dropping after the removal of part of the pus, but rising 
again within a few days. Emaciation, nightsweats, anorexia, diarrhea, 
etc., keep on; amyloid degeneration of the viscera, notably the liver, 
spleen, kidneys, and intestines, develops and the patient sooner or 
later succumbs to exhaustion. 

The suggestion of some authors that after removing the pus nitro- 
gen should be inflated into the pleura has been tried by the writer, 
not found to offer any advantages, and abandoned. 

Pneumothorax.— Considering the morbid anatomy of pneumothorax 
complicating pulmonary tuberculosis, it is clear that the prognosis 
is vere serious. Bearing in mind that the rent in the visceral pleura 
occurs in tuberculous tissue, its chances of cicatrization are remote. 
However, if the rent is small, intrapleural pressure and collapse of the 
lung, at times, help along in the direction of healing of the laceration, 
and we then may even have what some writers have called “ provi- 
dential pneumothorax;”’ the collapse of the lung results in a temporary 
or even permanent improvement in the general and local condition of 
the patient. But when the rent in the pleura is large, it remains open 
indefinitely and the morbid secretions of the lung lesion enter the 
pleural cavity through a pleuropulmonary fistula and infect it. 

The acute onset with shock, pain, dyspnea, ete., demands active 
treatment. The indications are clear: The patient is to be relieved 
of the urgent and menacing symptoms, his heart is to be stimulated, 
etc., which is best done by a hypodermic injection of morphine. But 
if the patient is not calmed, and the dyspnea is urgent, thoracocentesis 
is to be performed. This is often the only means at our command to 
relieve the extreme and agonizing dyspnea. ‘Tapping the air in the 
affected pleural cavity gives prompt relief, though unfortunately only 
of short duration in most cases. Plunging a hy podermic needle into 
the affected side is sufficient, because the expiratory pressure within 
the pleura is greater than that of the external atmosphere. It is good 
to attach a pibber tube to the needle by one end, while the other is 
placed in a pail of water, thus forming a water valve which permits 
the free exit of the air from the chest, but prevents its return. 


PNEUMOTHORAX 859 


If the relief thus obtained is only transitory, the operation is repeated; 
in some cases it may be necessary to repeat the tapping four, five, or 
even seven times during the first day. Some have tried to obviate 
this by inserting a cannula and leaving it in the chest wall for several 
hours or days; the rubber tube all the time in the water. But I have 
found it very difficult to retain the needle in place and to keep it aseptic. 
For this reason I prefer to make several punctures as the urgency of 
the symptoms demand. 

Many theoretical objections have been raised against tapping the 
chest in these cases. But one has only to witness a case in which the 
agonizing pain and air hunger are promptly relieved by tapping, to 
appreciate that this is the only measure which gives relief. As in 
urgent cases of any kind, theoretical considerations are left until the 
menacing symptoms are under control. In fact, after one tapping the 
patient begs for another when the dyspnea returns. 

I have recently been more successful with induction of counter- 
pressure within the pleura by injection of air in the way we do when 
inducing a therapeutic pneumothorax. This was first suggested by 
Morelli. It appears from actual measurements that in the vast 
majority of these cases the intrapleural pressure is negative, even 
though the patient suffers from severe dyspnea. Increasing the amount 
of air in the pleura the perforation is closed by the air pressure, the 
edges are held together and they soon heal. Closure of the fistula 
prevents further entry of septic matter from the lung into the pleura. 
As done by A. Pisani,! a needle connected with a manometer is intro- 
duced into the pleura and, if the pressure is found positive, some of 
the air is withdrawn. Then the tube leading from the needle is con- 
nected with the usual pneumothorax apparatus and air is allowed to 
enter the pleural cavity until the manometer registers 5, 10, or even 
20 cm. positive water-pressure. 

In several cases in which this method was tried by the writer, relief 
was noted immediately in two out of three. In some cases we may 
continue the pneumothorax treatment, just as we do in cases of thera- 
peutic pneumothorax. 

We meet with cases in which the embarrassment of the circulation 
and respiration continues in spite of repeated tappings, or introduction 
of air, and the prognosis is gloomy. The causes are not primarily 
mechanical, but physiological. The opposite lung is congested and 
the circulation is thereby more embarrassed than by the displacement 
of the mediastinum. In these cases we may try oxygen inhalation, 
and cupping all over the posterior aspect of the chest. Some use wet 
cups or venesection to relieve the right ventricle which is becoming 
paralyzed from extreme overdistention. “I have no doubt,” says 
West, “that life might be sometimes saved by timely venesection, and 
it is certain that bleeding is not so much employed in these urgent 
cases as it ought to be.” 


1 Gazzetta degli Ospadali e delle Clinicehe, 1917, 37, 379. 


860 TREATMENT OF COMPLICATIONS 


The heart action is to be sustained by large doses of digitalis, 
spartein or camphor. 

In milder cases, especially those in which the pneumothorax is only 
partial and the symptoms are not so urgent, the treatment is less 
vigorous. The dyspnea, pain, and distress are usually controlled by 
a dose of morphine hypodermically, and within a day or two the patient 
feels quite comfortable. Partial pneumothorax is very frequent in 
tuberculous patients, and commonly is followed by improvement in the 
tuberculous lesion in the lung. 

The after-treatment, if the patient survives three or four days, is 
that of the underlying tuberculous process in the lungs. Inasmuch 
as the pneumothorax, with its sudden onset and agonizing symptoms, 
often leaves the patient in a debilitated condition, rest and proper 
feeding are to be enforced. In rare cases the pneumothorax, acute 
and menacing as it was at the onset, turns out to be “providential,”’ 
as some French authors say. The collapsed lung is given an oppor- 
tunity to heal and recovery may take place ultimately. Some recom- 
mend that in such cases the pneumothorax should be continued by 
injections of nitrogen in the approved manner. 

After the menacing symptoms have abated, the patient, regaining 
his strength and composure, provided he has no fever, may be per- 
mitted to leave his bed and take mild walking exercises. We know 
now from experience with artificial pneumothorax that one can do 
considerable exercise, or even work, while one pleural cavity is filled 
with air and the lung collapsed. 

Hydropneumothorax.—The treatment of effusion into a pleural 
cavity filled with air is conservative, just as that of pneumothorax. 
The fluid is absorbed sooner or later spontaneously. We now have 
experience with this condition in cases with artificial pneumothorax. 
So long as there is no fever or dyspnea, the patient may be allowed 
considerable exercise. But in case the intrathoracic pressure becomes 
high and produces dyspnea when the patient is at rest, the pressure 
must be reduced. This can be done by withdrawing some of the air 
or fluid. The latter is the best. With an aspirating apparatus a 
part of the exudate is withdrawn. In many cases the operation has 
to be repeated. In favorable cases this withdrawal stimulates the 
absorption of the rest of the fluid. In several cases I have had good 
results with autoserotherapy (p. 857). 

Pyopneumothorax.—The treatment of this complication is very 
unsatisfactory. Operative interference has not given encouraging 
results. At best, a fistula is left in the chest which discharges pus 
indefinitely. The ultimate result is worse than when only tapping of 
the pus is resorted to. The indications, therefore, are to aspirate the 
pus at frequent intervals with a view of keeping the patient afebrile 
as far as possible. The bacteriological findings have no influence on 
the prognosis and treatment, as has already been stated when speaking 
of empyema complicating phthisis. 


LARYNGEAL TUBERCULOSIS S61 


Laryngeal Tuberculosis.—Many cases of tuberculous laryngitis 
show a strong tendency to spontaneous cure, especially in patients 
whose lung lesion also manifests a tendency to improvement. In fact, 
the progress of the lesion in the larynx goes hand-in-hand with the 
progress of the Jung lesion, though the physical signs of the latter are 
apt to be obscured by the former. This is clearly seen in cases in which 
the induction of a therapeutic pneumothorax is effective in curing the 
patient. If there has been a laryngeal lesion it often shares in the 
general improvement of the patient. 

In my experience, local treatment is not often effective in enhancing 
cicatrization of laryngeal lesions. When carried out vigorously, it is 
apt to do harm. The application of local escharotics and cauteriza- 
tion has been harmful in the long run, or of no benefit in the vast 
majority of my cases. As has been pointed out by St. Clair Thomson,! 
lactic acid, which is the favorite drug used by laryngologists, is unavail- 
ing except in strength of 50 per cent or more. Hence, sprays of 2 per 
cent are nothing but irritating. Frequent applications are also 
irrational, the object being to produce an eschar which does not separate 
for one or three weeks. When the slough is detached a healing ulcer is 
exposed; but there are generally deeper deposits, requiring a repetition 
of the cauterizing process, so that four to twelve applications may 
have to be spread over as many months. The use of a 20 to 25 per 
cent solution of argyol, or a 2 per cent solution of methylene blue for 
local application, is less likely to be painful or harmful. Where the 
mucous membrane is unbroken no local application of drugs does any 

ood. 

The futility of local applications of any kind in superficial tubercu- 
lous lesions is clearly seen in tuberculous lesions of the skin. Derma- 
tologists are not so sure of promoting a healing process by the applica- 
tion of escharotics to lesions of lupus, as are laryngologists in tuber- 
culosis of the larynx. I have often felt that my patients had better 
chances of recovery before local treatment of laryngeal lesions was 
applied than after vigorous treatment. 

In a few cases I have seen excellent results when the patient ceased 
talking altogether, thus affording perfect rest to the larynx. But it 
must be done thoroughly. The patient should have a pad and pencil 
and carry on all conversation in writing. In the cases, mostly women, 
in whom this treatment was carried out perfectly, the laryngeal lesion 
healed. There are, however, few patients who have sufficient will 
power and perseverance to continue this treatment for a long time. 
In patients with advanced and active lesions in the lungs, there is no 
reason for trying it, because they are doomed anyway. 

As has been shown by Fetterolf,? there is one form of the disease 
in which unlimited use of the voice is advisable, this being the variety 
in which the vocal cords are the only parts of the larynx involved. 


1 Diseases of the Nose and Throat, New York, 1912, p. 606. 
2 Hare’s Modern Treatment, Philadelphia, 1911, 2, 402. 


862 TREATMENT OF COMPLICATIONS 
This is commonly called the “chorditic’ form, the cords appearing 
slightly congested and having on their upper, and to a slight extent 
on their mesial aspect a number of reddish granular growths. ‘These 
are possibly sometimes submucous tubercles, but more frequently 
are distended mucous glands with their duct orifices occluded. Vocal 
exercise aids in clearing up the condition, and it is in this form that 
improvement of the voice so frequently follows an acute coryza. 

In all cases with dysphagia palliative treatment must be applied. 
We may try to obtain relief by laryngeal insufflations of 3 to 5 grains 
of orthoform or anesthesin. It is only effective when there is ulceration 
and the powder remains on the ulcer. If given about one hour before 
the main meal the patient may be comfortable for a whole day. The 
following formule may also be used: 


R—Orthoformi 5 A TE ae Be ee Pte es DO On 2.0 
Todofornal). fey ee ee, Pee no Te PARO) 
Mentholi <2 h./" 2 Reet ee ee eer any 0.4 

M. S8S.—Insufflate a few grains one hour before meals. 

R—Cocaine hydrochloridi os minke shuets Meraie meer Te OTs x Ona 
Morphinzethydroculoridiye sateen oan Oat 
Mentholis: er ice ee bee eee ae ory 10 
Todofonmig yale se eee Se eel) 8.0 
Acidi borici AP 5 ij 8.0 


M. 8.—Insufflate a few grains one hour before meals. 


The application of these powders is to be made with special insuffla- 
tors. They are designed so that the spray goes vertically downward, 
not backward into the pharynx. 

In some cases the dysphagia is severe and not at all influenced by 
the application of remedies locally. Injections of alcohol into the 
superior laryngeal nerve may then be tried. Relief from pain may be 
obtained lasting several weeks. Rudolf Hoffmann was the first to 
suggest this mode of treatment. The technic of the injection is thus 
given by J. Dundas Grant?! 

Place the patient in a horizontal position and, with the thumb of 
the left hand, press the sound side of the larynx toward the middle 
line so that the affected half projects distinctly; the other fingers of 
the hand lie on this. The index finger enters the space between the 
thyroid cartilage and the hyoid bone from without until the patient 
announces that a painful spot had been reached. With a little 
practice one arrives at it at the first go-off, when one has become 
familiar with the topographical relations. Now the nail of the index 
finger is placed on the skin (which has been previously disinfected) 
in such a way that the point of entrance for the needle lies opposite 
its middle. The needle is pushed in for about 1.5 em. and this distance 
is marked off on the needle perpendicular to the surface of the body. 
According to the thickness of the subcutaneous layer of fat, the 


1 Lancet, 1910, 1, 1754. 


LARYNGEAL TUBERCULOSIS 863 


perforation has to be more or less deep. The needle is then carefully 
moved so as to seek a spot at which the patient states that he feels 
painintheear. The syringe filled with 85 per cent alcohol warmed to 





Fic. 128.—The thyrohyoid region. (Grivot.) 





Cricoid carlilage- 


Fic. 129.—Space where to insert the needle for producing anesthesia of the superior 
laryngeal nerve. (Celles.) 


864 TREATMENT OF COMPLICATIONS 


the temperature of 45° C. (113° F.) is screwed on to the handle and 
the piston is then slowly pressed down. ‘The patient now feels pain 
in the ear, the passing off of which he indicates by raising his hand. 
During the operation he has to avoid both swallowing and speaking; 
if, however, he makes a movement of swallowing we must follow the 
movement of the syringe with a light touch. The injection is kept up 
until no further pain occurs in the ear; then the needle is removed and 
collodion or adhesive plaster is placed on the spot of the injection 
without pressure. The needle employed should be one with a point 
bevelled off much more obtusely than in an ordinary hypodermic 
need!e, so as to avoid the risk of puncturing a vessel. 

I have tried this method in many cases and obtained relief for the 
patients in about 50 per cent. Failures are due to missing the nerve, 
which is unavoidable in many cases. 

There are cases in which all the above fail to relieve the sufferer, 
and all we can do is to give large doses of anodyne drugs. In some we 
may obtain relief by helping the patient in the following manner while 
he eats: A trained person stands behind the patient and makes firm 
and even pressure at the angle of each jaw at the moment of swallow- 
ing. Another way is known as Wolfenden’s position: The patient 
lies prone over the bed with the face over the end and sucks the nourish- 
ment through a glass tube from a cup held by an attendant or placed 
on the floor. ‘These maneuvers seem cumbersome, to say the least, 
but when having under our care a patient who cannot swallow even 
water without severe pains in the throat, we are ready to try anything. 

There remains yet to mention the various operations of curettage 
and cautery which laryngologists perform in these cases. Some 
employ direct laryngoscopy while operating, but this is not only violent, 
but the results have been disastrous in all the cases that have been 
done for me. In advising operation to a patient of this class we 
must first ascertain the general and the local condition of the lungs. 
In case the prognosis is poor because of the general condition, there is no 
reason for operating. I always object to operations in febrile and 
cachectic patients. 


INDEX OF AUTHORS. 


A 


ABDERHALDEN, 116 
Adami, 63, 107 

von Adelung, 800 
Albrecht, 107 
Aldrich, 508 
Alexander, 394, 553 
Allard, 513, 518 
Allbutt, 487, 727 
Als, 824 
Amenomiya, 565 
Ameuille, 509 
Amrein, 295 
Amstel, 580 

Ancell, 62, 257 
Anders, 234, 241 
Anderson, John F., 57, 207, 285 
Andral, 122, 240, 339, 598 
André, 45 

Andrews, 108 
Antylus, 755 
Aretaeus, 241, 302 
Arkin, 754 

Arloing, 41 

Arluck, 44, 451 
Armand-Dellile, 662 
Arneth, 283 
Arnould, 621 
Arnsperger, 363 
Asearelli, 638 
Aschoff, 169 

Ash, 534 

Assmann, 357, 363 
Atwater, 740 
Auche, 108 
Aufrecht, 53, 126, 149, 325 
Ayer, 175 


Bases, 45 

Baccelli, 617 

Bach, 522 

Bacmeister, 50, 53, 118, 121, 139, 391 
Balboni, 807, 813 

Baldwin, 24, 38, 111, 114, 668, 763 
Ballenger, 559 

Balzer, 555 

Bamberger, 287 

Bandelier, 344, 389, 415, 766 


55 


Bang, 110, 780 

Barbier, 286, 314 

Bard, 415, 419, 524 
Bardswell, 216, 276, 621, 724, 745, 767 
Barjon, 496 

Barnes, 754 

Barot, 467 

Barrel tle 

Bartel, 50, 115, 148, 156, 455, 583, 610 

716 

Barth, 589 

Barthez, 594 

Bartlett, 57, 63 

Bartlett, J. R., 150 
Barwell, 558, 561 
Pateman, 741 

Bauer, 114, 123, 610 
Baumann, 140 
Baumgarten, 53, 106, 153, 161, 163 
Bayle, 368, 419, 512, 558 
Beale, 223 

Beck, 390 

Béclére, 565 

Beddoe, 299 

Behrend, 387 

Behring, 59, 142, 662, 770 
Beitzke, 41, 52, 55 

Bell, 525 

Benda, 437, 568 
Benedict, 698 

Bennett, 257 

Bergel, 715 

Bergheim, 112 

Bernard, 44, 835 
Bernard, Claude, 349 
Bernheim, 662 

| Bertillon, 81 

| Besredka, 392 

Bezangon, 314, 415 
Biach, 523 

Bialokur, 609, 612 

Bikb, 362 

_Bickersteth, 794 
'Biermer, 405 

| Biggs, 81, 692 

Binet, 112 

| Birch-Hirschfeld, 52, 69, 109 
| Bisaillon, 8438 

| Bisbee, 648 

| Bittorf, 521 

| Black, 272 

‘Blake, 462 


866 INDEX OF 

Blakiston, 514 

Bloomfield, 598 

Blum, 287 

Blumberg, 523 

Blumenfeld, 282 

Boardman, 206, 362 

Boas, 290, 556, 593, 596 

Bodington, 696 

Bohland, 280, 592 

Bollog, 584 

Bonney, 314, 562, 787 

Borel, 74 

Borschke, 566 

Boston, 383, 414 

Bowditch, 512 , 

Bowlby, 471 

Bramwell, 514 

Brandenburg, 609 

Brauer, 602, 795, 798, 800, 819, 822 

Bray, 214, 215, 220, 340, 343, 349 

Brehm, 284 

Brehmer, 111, 231 

Brieger, 260 

Broders, 614 

Bronfenbrenner, 392, 511 

Brooks, 662 

Brown, 24, 47, 265, 411, 598, 766, 769 

Brown, E., 474, 477 

Brown, Wm. G., 669 

Brownlee, 42, 59, 98, 129 134, 154 

Brown-Séquard, 249 

Bruce, 420, 680 

Briickner, 387 

Brunon, 149 

Brunton, 724 

Budd, 257 

Bullock, 832 

Bulstrode, 128 

Burnand, 63, 68, 226 

Burns, 23, 242, 265 

Bushnell, 34, 97, 127, 158, 189, 284, 339, 
346, 352, 664, 668 

Busse, 598 


C 


Caxor, 243, 246, 351 
.Calmette, 47, 55, 56, 73, 144, 389, 392, 
666 
Calvin, 786 
Capps, 2938, 483, 484 
Carr, 132, 455 
Carrel, 826 
Carrington, 682 
Carroll, 394 
Carson, 794 
Castaigne, 524 
Castellani, 551 
Cattermole, 71 
Cavagnis, 107 
Celles, 863 
Cepulic, 394 
Cetrangalo, 856 
Chalier, 109 





AUTHORS 


Chalmers, 552 
Chamaro, 602 
Chamberland, 108 


_Chambers, 62 
/Chantemesse, 480, 511, 569 


Chapin, 728 

Chapman, 216, 734, 745 
Charvot, 574 

Chauvet, 379 

Chiari, 555 

Childs, 363 

Chittenden, 739 
Claisse, 612 


| Clark, Andrew, 257, 371, 419, 421, 580 


Clark, James, 257 
Claypole, 257 
Clemenger, 210 
Clough, 285 
Clouston, 294 
Clovis, 598 


| Cobb, 118 


Cobbett, 34, 41, 56, 68, 130, 140, 142, 
158, 685 


' Cochrane, 769 

| Cohen, M. Solis, 267, 290, 556 
Cohen, S. Solis, 114, 604, 608 
Cohn, 361, 362 


Collis, 133, 134, 135, 863 
Combe, 294, 449, 739 
Condie, 234 

Coonley, 663 

Coriveaud, 514 

Cornet, 23, 46, 68, 133 
Cornil, 290, 589 

Corper, 135, 140, 255, 272, 276, 754 
Cotton, 22, 56 
Councilman, 57 
Courcoux, 480, 511 
Courmont, 45, 836 


_Couston, 513 


Cowan, 530 

Cowie, 109 

Craig, 282, 392, 393 
Cramer, 136 
Crofton, 112 


| Cruice, 564, 573 
_Cruveilhier, 589 


Cullen, 579 


'Cummer, 532 


Cummings, 697, 700, 701 
Cummins, 74 

Cursham, 569 

Curtin, 757 

Czerny, 592 


| Cayhlar, 592 


D 


Da Costa, J. C., 465 
Da Costa, J. M., 324 
Dakin, 826 
Damman, 42 


| Daremberg, 220, 434, 7438, 477 
| Darier, 269, 270 


Dastre, 785 


laa teas Ria i 


INDEX OF 


Davies, 843 
Davis, 27 
Debains, 392, 629 
Debove, 734 
Dehn, 363 

Deibel, 580 
Delafield, 174 
Deléarde, 144 
Delépine, 23 
Delhern, 189, 535 
Dellile, Armade, 000 
Delpeuch, 299 
Demme, 663 
Demoiseau, 491 
Deneke, 44 

De Renzi, 754 
D’Espine, 466 
Destrée, 290 
Dettweiler, 218, 737, 772 
De Witt, 749, 750 
Dieulafoy, 245 
Dioscorides, 754 
Doane, 22 

Dobell, 257 
Dobrovici, 657 
D’Oelsnitz, 290 
Dold, 45, 284 
Donaldson, 495 
Dorset, 21 
Dowdell, 569 
Doyen, 355 
Drasche, 523 
Drummond, 739 
Duboff, 683 
Dubrull, 513 
Duckworth, 599 
Dumarest, 829, 833, 840 
Dunham, 362, 493 
Duplay, 574 
Diirek, 50 
Dworetzky, 558, 559 
Dzierzgowski, 116 


Eastwoop, 19 

Eden, 57 

Ehrlich, 510, 747 

Eich, 580 

Einhorn, 260 
Elderton, 150, 624, 647 
Eliasberg, 395, 586 
Ellis, 491 

Emerson, 524 
Emerson, Haven, 588 
Engel, 294 
Engelmann, 48 

Ernst, 44 

Escherich, 455 

Estor, 638 

Etiénne, 569 

Evans, 295 

Ewart, 174, 314, 351, 409, 465, 574 
Ewing, 588 





AUTHORS S67 


FaaInout, 836 

Faisans, 279, 612 

Farrago, 395 

Felner, 580 

Fenwick, 199, 257, 260 
Fenwick, W.S., 257 

Féré, 122 

Fernet, 510 

Fetterolf, 322, 683 

Fildes, 392 

Findel, 140 

Finkler, 539 

Fisac, 133 

Fischer, 285 

Fischera, 551 

Fisher, 740 

Fleiner, 479 

Fleischner, 663 

Flexner, 550 

Flick, 784 

Flicker, 479 

Fleissinger, 716 

Flint, 254, 323, 512, 514, 618 
Floresco, 785 

Florschiitz, 648 

Floyd, 481, 818 

Fliigge, 46, 48, 49, 698 
Fochi, 784 

Folin, 739 
Fontana-Tribeudeau, 552 
Foot, 163 

Forchammer, 584 

Fordyce, 157 

Forget, 598 

Forlanini, 795, 797, 804, 829, 837 
Forssner, 581, 583 

Forster, 584 

Forsyth, 759 

Fowler, 171, 555, 615, 763, 766 
Fox, 195, 234, 253 
Fraenkel, 770 

Fraenkel, A., 535 

Fraenkel, C., 45, 140, 295 
Frangois-Frank, 249 

Franz, 390 

Fraser, 40 

Fraser, Thompson, 154, 711 
Freudenthal, 561 

Freund, 118, 139, 580 
Frey, 785 

Freymuth, 149 

Frias, 70 

Friedmann, 29, 31, 106, 657 
Friedrich, 405 

Frieseke, 535 

Frischauer, 553 

Fulton, 97 

Funk, 234, 257, 261, 286, 534 
Fussell, 522 


G 
GaBB, 522 
Gabbet,t19 


S6S INDEX OF 


Gaffky, 57 

Galen, 255, 302, 755 
Ganghofner, 387 
Garb, 133 

Gardner, 141, 153 
Garland, 491 
Garnier, 663 
Garrahan, 70 
Gartner, 106 
Garvin, 539 
Gassmann, 261 
Gaube, 112 

Geddes, 124 

Geipe, 108 
Geisbock, 281 
Gerhardt, 250, 535 
German, 486 

Ghon, 57, 108, 168, 450 
Gibson, 468 

Gibson, Cole B., 394 
Giesmann, 804 
Gilbert, 140, 283, 410, 614 
Gillet, 539 

Gilliland, 362 
Gilmore, 272 
Gimbert, 578 
Giraux, 638 
Glaister, 83 

Glaser, 392 

Glover, 392 

Goebel, 50 

Goethe, 253 

Goetz, 613 
Goldscheider, 314, 331, 336 
Goldtwait, 123 
Goodale, 143 
Gordon, 48 

Goring, 150 
Gornault, 153 
Goujot, 574 

da Gradi, 883 
Graetz, 210 
Graham, 525 
Gramen, 395 
Grancher, 257, 314, 337, 465, 789 
Grant, 126 

Grasser, 44, 639 
Grassmann, 44 
Grau, 638, 639 
Graves, 608 
Grawitz, 282, 479 
Gray, 526, 570, 832 
Greene, 648 
Greenfield, 207, 608, 609 
Gregg, 140 

Griffith, A. 8., 20, 33, 34, 40, 64, 68 
Griffith, F., 64 
Grivot, 863 

Grober, 479 

Grocco, 602, 493 
Grysez, 56 

Guerin, 144, 668 
Gutstein, 812 
Guyenet, 564 

Gye, 136 


AUTHORS 


Haun, 638 

Halbron, 313 

Haldane, 698 

Hall, D. C., 703 

Hall, F. De Haviland, 244 
Halter, 133 

Halverson, 112 
Hamburger, 608 
Hamburger, F., 37, 49, 57, 76, 121, 388, 

472 

Hamman, 390, 391, 513, 522, 539 
Hammer, 392 
Hanau, 581 
Hanford, 611 
Hanot, 589, 614 

Hans, 539 
Hansemann, 138, 368, 765 
Hansen, 110 

Harbitz, 51, 63, 64, 148, 443 
Harras, 118, 121 
Harrington, 296, 530 
Harris, 223 

Hart, 69, 118, 121, 139 
Hartley, 566, 570 

Haupt, 150 

Haushalter, 569 

Haven, 283 

Hawes, 351, 558, 640 
Hayek, 621 

Hayem, 260 
Head, 289 

Head, Henry, 292 
Heberden, 274 
_Hedenburg, 748 

Hedges, 513 

Hefflebower, 629 

Hein, 231 

Heise, 24 

Hellin, 526 

Helmers, 754 
'Hempelmann, 451 
Henderson, 286 
Henderson, John T., 573 
Henke, 181 
Herard, 589 
Hermann, 205 
Herter, 739 

Hess, 49, 58 

Heublein, 469 
_Hierokles, 569 
_Hilderbrand, 107 

Hill, Leonard, 698 
Hillenberg, 72 
| Hinsdale, 715, 720 
Hippocrates, 61, 128, 299, 502, 580 
| Hirsch, 76 
Hirtz, 570 
| His, 120 
Hofbauer, 553 

| Hoffman, 74, 77, 78, 80, 91, 132, 133 
_Holeman, 123 

Holst, 359 
| Holt, 44 








Honeij, 467 

Honl, 109 
Honsele, 638 
Hoppe-Seyler, 477 
Horetzky, 638 
Howell, 467 
Hrdlicka, 73 
Huber, 296 
Humphrey, 571 
Hunter, 569 
Hutchinson, 257 
Hutchinson, Woods, 73 


IGERSCHEIMER, 32 
Inman, 392, 694 
Iscovesco, 759 
Iselin, 574 

Iwai, 128 


* 


JACCOUND, 632 
Jackh, 107 
Jackson, 551 
Jacob, 72 
Jacobaeus, 835 
Jacobson, 296 
Jacoby, 210 
Jadassohn, 271, 584 
Jakowski, 510 

von Jaksch, 211 
James, 51 

James, T. L., 716 
Jani, 107 
Janowski, 258 
Jeannil, 638 
Jeannin, 268 
Jelliffe, 295 

Jessen, 392, 617, 820 
Jex-Blake, 248, 542 
Jochmann, 602 
Jones, 51 

Jordan, 359 
Joseph, 210 
Jupille, 392, 629 


KAMINER, 580 
Keats, 786 

Kehl, 608 

Keith, 122 
Kellogg, 738 
Kelly, 484 
Kelynack, 614, 615 
Kenchington, 645 
Kennerknecht, 284 
Kernig, 441 
Kessel, 276, 285, 391 
Kettle, 136 


INDEX OF AUTHORS 869 


Keysser, 126 

Kidd, Perey, 514, 558, 599 

-IGenbéck, 530 

KGewe, 580 

| Kindberg, 189, 511, 535 

| King, 736 

) King, J. To ss5t 

Kinghorn, 626 

Kitassato, 58 

| Kjerrulf, 111 

Klebs, 33 

Klemperer, 152, 260, 822 

Klenke, 24 

| Klimmer, 764 

Kline, 563 

Klipstein, 50 

Klotz, 186, 329 

| Knight, 718 

'Knipfelmacher, 451 

| Koch, Herbert, 451, 453 

| Koch, Max, 29 

_Koch, Robert, 17, 29, 46, 95, 145 

| Kocher, 608 

Kohler, 579, 705 

Kohlisch, 46 

| Konig, 638 

| Koniger, 515 

| Koplik, 470 

Koranyi, 465 

Koslow, 284 

Kossel, 58 

| Koster, 513, 518 

Kraus, F., 582 

Krause, Allen K., 24, 145, 361, 363, 447, 
579, 683 

Kreuscher, 832 

Kreutzfuchs, 359 

Kronig, 314, 327, 329, 537 

Krumwiede, 28, 33 

Kruse, 29 

Kuban, 132 

Kupferle, 580 

Kurashige, 284 

Kiiss, 168, 392, 747 

Kuthy, 30, 111, 201, 237, 411 





L 


| LAENNEC, 62, 144, 241, 368, 396, 512, 618 
Lafitte, 114 
Laignel-Lavastine, 114 
Lamallerée, 29 
Lancereaux, 614 
Landis, 581, 583, 615 
Landouzy, 299, 510 

| Lange, 30, 32, 564 
Langstroth, 292 

Lanz, 394 

Lasbennes, 580 
Laschtchenko, 48 
Latham, 105, 724 
Lauritz, 261 

Leaming, 346 

Lebert, 564, 580 





870 INDEX OF 

Lee, 698 

Lees, 314, 379 

Lehmann, 108 

Lemgey, 638 

Lemke, 832 

Lémoine, 603 

Lenglet, 584 

Leplat, 674 

Leredde, 392 

Lésague, 258, 571 

Lesne, 569 

Lesieur, 45 

Létulle, 172, 173, 297, 522, 578, 612 

Leube, 729 

Leudet, 411 

Levaditi, 157 

Levene, 36 

Levison, 257 

Levy, 150, 156, 281 

Levy, F., 313 

Lewandowsky, 45, 271, 584, 585 

Lewis, 741, 749 

Leyden, 568 

Libman, 249 

Lichtheim, 249 

Liebermeister, 284, 569 

Limbeck, 282 

Lindhagen, 89 

Locke, 276 

Loeffler, 207 

Lombard, 62 

Lombardi, 301 

Lombroso, 122 

Londe, 109 

Longa, 510 

Longet, 249 

Longstrath, 292 

Loomis, 371 

Lord, 253 

Lorentz, 614 

Lorrain, 539 

Louis, 195, 232, 234, 253, 523, 564, 569, 
598 

Lowenstein, 29, 42 

Lubarsch, 52, 53, 63, 108, 134, 614 

Lundborg, 123 

Lunde, 786 

Luschka, 317 

Lustgarten, 30 

Lyon, 816 


McCann, 113 
McCarthy, 253 
McCartney, 794 
McCaskey, 615 
McConkey, 143 
McCrae, 63, 171, 534 
MelIntosh, 392, 393 
McLean, 692 
MeNeil, 154 
McSweeney, 724, 731 
Mace, 483 





AUTHORS 


Macfadyen, 134 

Macht, 21, 247, 784, 785 
Mackenzie, James, 483 
Mackenzie, Morel, 558 
Mackenzie, Hector W. G., 765 
MacWhinnie, 702 
Maffucci, 23, 25, 106 
Magnus-Alsleben, 238 
Magnus-Levy, 605 
Mahler, 22, 112, 257, 261 
Mallory, 57 

Mandl, 793 

Mann, 593 
Mannheimer, 786 
Manning, 71 
Manoukhine, 392, 630 
Mantoux, 70, 229 
Manwaring, 511 
Maragliano, 600, 770 
Marcellus-Empricus, 755 
Marcet, 284 

Marcus, 41 

Marfan, 260, 663 

Marie, 275, 716 
Marmoreck, 770 
Marquard, 579 

Martius, 155 

Massol, 392 

Mathieu, 657 

Matson, 843 

Mauthner, 115, 611 
Maximow, 163 

Mayer, 152 

Mayo, 152 

Mays, 618 

Meader, 20 

Means, 813 

Melchior, 261, 613 
Meltzer, 813 

Mendel, 739, 741 

Meriel, 565 

Metchnikoff, 73, 674, 739 
Mettetal, 39, 391 
Metzger, 629 

Meyer, A., 210, 530 
Meyer, K. F., 663 
Meyer, Willy, 841 
Microli, 617 

Milchner, 106 

Milian, 600 

Miller, H. R., 392, 630 
Miller, J. L., 539, 775 
Miller, William Snow, 479 
Mills, 286, 573, 598 
Mioche, 70 

Mitchell, 34, 154 
Mitchell, Weir, 796 
Moeller, 111, 112, 195, 253 
Mohr, 126 

Moller, B., 32, 49, 153 
Moneanny, 114 
Mongour, 150, 569 





| Monkenberg, 69 


Montaugh, 393 
Montgomery, 276, 286, 287, 580, 605 


INDEX OF 


Moore, 78, 217 
Morelli, 831, 859 
Morgan, 801, 818 
Morgenroth, 151 
Morin, 114, 608 
Moritz, 134, 800 
Morland, 221, 766 
Moro, 44, 71, 388 
Morris, 493 

Mortley, 210 

Morton, 197, 263, 602 
Mosenthal, 573 
Mosiman, 608 
Mowat, 360 

Much, 20, 41, 153 
Mudd, 126 

Miller, B., 241 
Miller, F., 50 

Miller, Hans, 783 
Munoyerro, 70 
Miinstermann, 566 
von Muralt, 114, 291, 589, 716 
Murard, 829, 833, 840 
Murphy, 295, 808, 832 
Miisemeier, 42 
Musser, 304 

de Mussy, 280, 483 





N 


NA&GELI, 63, 68 
Nakari, 107 
Nattan-Larrier, 172, 173 
Naunyn, 605 

Neelsen, 19 

Nehring, 82 

Neisser, 46 

Netter, 510 

Newman, 116, 121, 247 
Newsholme, 128, 132, 729 
Nikolski, 521, 522 
Nocard, 25 

Nolf, 551 

Norris, 332, 580, 581, 583 
Nothnagel, 235 

Novack, 108 








O 
OESTREICH, 323 
O’Farrell, 252 
Ogle, 91 
Oliver, 110 
Opie, 66, 68, 414, 521 
Ormsby, 267, 268 
Orth, 41, 57, 156, 642 
Osborne, 739 
Osler, 513, 553, 554, 724 
Otis, 189 
Ottenberg, 249 
Overland, 72 


Pager, 496 
Paget, 584 





AUTHORS 871 


Paillard, 197 

Palmer, 580 

Pankow, 580 

Papavoine, 62 

Papillon, 289 

Pappenheim, 29 

Parfitt, 626, 727 

Park, 18, 22, 26, 27, 28, 33, 40 

Parr, 580 

Parrot, 168 

Pasquera, 46, 48 

Paterson, 511, 693 

Patzold, 44 

Pawlow, 741 

Pearce, 57 

Pearl, 96, 104 

Pearson, 62, 93, 96, 104, 105, 110, 150 
728 

Pehu, 109 

Pensunti, 510 

Penzold, 220, 678 

Peretz, 351 

Peron, 774 

Perry, 647 

Peter, 197, 199 

Peters, L. 8., 564, 602 

Peters, W. H., 578 

Petersen, 555 

Peterson, 482 

Petri, 27, 30 

Petroff, 21, 24, 47 

Petruschky, 150, 391, 600 

Pettit, 592, 601 

Pfannenstiel, 30 

Philip, R. N., 328 

Philip, W., 257 

Philippi, 766 

Pidoux, 598, 603 

Pierce, 513 

Piéry, 233, 269, 314, 420, 624, 800, 832 

Pietrzikowski, 638 

Piller, 89 

von Pirquet, 71, 128 

Pisani, 859 

Plesch, 320, 406 

Plummer, 609 

Polanski, 122 

Pollack, 257, 603 

Pollak, 70 

Poncet, 602 

Pope, 150, 411 

Porter, 103 

Porter, A. S., 116 

Porter, William, 780 

Potain, 287 

Pottenger, 122, 266, 307, 313 

Poujade, 690 

Powell, 281, 371, 495, 523, 525 

Power, D’Arcy, 599 

Pradal, 313 

Preissich, 391 

Price, 246 

Prudden, 174 

Prudella, 580 


QUERNER, 285 
Quryat, 449 


R 


RaBINOWITSCH, 29, 30, 41, 69, 144, 156, 
391, 764 

Radcliffe, 392, 601 

Radziejewski, 387 

‘“Ramond, 490 

Randt, 395 

Ransome, 91, 98, 126, 128 

Raphael, 207 

Rasmussen, 176, 253 

Rautenberg, 833 

Ravenel, 52, 53, 54, 57, 285 

Raw, 238, 604 

Real, 834 

Regnault, 592 

Regner, 834 

Reibmeyr, 298 

Reiche, 237, 241, 580, 602 

Reichenbach, 749 

Reinecke, 395 

Reinhart, 64, 68 

Reinhart-Goodwin, 255 

Rénon, 114, 656, 747, 834 

Reuben, 451, 453 

Reuschel, 387 

Revault, 569 

Ribbert, 53, 139 

Richet, 738 

Riddell, 530 

Riesman, 522, 

Riess, 408 

Rietschel, 108 

Rilliet, 594 

Rindfleisch, 118 

Ringer, 785 

Risel, 63 

Rist, 189, 511, 535, 667, 800, 802, 838 

Ritter, 153 

Rivers, 123 

Riviere, 154, 314, 336, 340, 379, 766 

Rivolta, 25 

Robin, 112, 286, 729 

Robinson, Beverley, 752 

Robinson, Samuel, 574, 842 

Roger, 44, 48 

Rogue, 290 

Rokitansky, 116, 580 

Roland, 510 

Rolleston, 614 

Rolly, 388 

Romanowski, 552 

Romer, 48, 54, 60, 109, 145 

Rondot, 756 

Ropke, 344, 289, 415, 766 

Rosalino, 123 

Rosenau, 58 

Rosenberg, 716 

Rosenberger, 148, 284 

Rosenfeld, 82 


539 


INDEX OF AUTHORS 


_ Rosignol, 145 
Rossalimo, 123 
Rossel, 824 
_Rosthorn, 580 
Rousseau, 253 
Roux, 25 
Rubel, 687 
Rubinstein, 392 
Ruedinger, 410 
| Ruge, 569 
Rumpf, 770 
Ruscher, 645 
Russell, 112 


SAATHOF, 609 
Sabourin, 221, 229, 556, 580 
Sabrazes, 569 

'Sahli, 763 

St. Aude, 291 

St. George, 614 
Sainton, 313 

Sajet, 89 

Sajous, 114 

Sale, 522° 

Salters, 233 

Sampson, 365, 565 
Sander, 40 

Sands, 616 

| Sauerbruch, 826, 841, 843 
Saugman, 144, 227, 798, 800, 836, 839 
Sawyer, 465 

Saxe, 295 

Saxtorph, 793 

'Sazuki, 284 

Schade, 581, 583 
Schiffer, 581, 583 
Schaffle, 265 

Schauta, 580 

Scheel, 63 

| Scheppelmann, 522 
Scherer, 611 

| Schern, 284 

Schick, 451 

Schiff, 395 

| Schlachter, 104 
Schlimpert, 577 
Schlossberger, 31, 32 
Schlossmann, 81 
Schliitter, 104 

Schmidt, 39 

Schmorl, 52, 108 
Schréder, 22, 56, 653, 720, 767 
Schule, 522 

Schulze, 121 

Schwatt, 276 
Schweitzer, 519 

Scott, 573 

Sears, 512 

Sedlmayr, 804 

Selter, 82, 140, 156, 210 
Senator, 287 
Serbonnes, 398 





INDEX OF AUTHORS 873 


Sergent, 291, 338, 353, 381, 486, 556, 599, | Tecklenberg, 580 


612 
Sewall, 314, 381, 713 
Shingu, 796 
Shortle, 787 
Sieber, 116 
Simmonds, 107 
Simon, 211 
Singer, 337 
Siredey, 612 
Sitzenfrey, 108 
Sluka, 464 
Smith, 121 
Smith, Eustace, 451, 467 
Smith, F. C., 719 


| Tecon, 22 

Tendeloo, 117, 178 
Tenzer, 388 

Tesler, 580 

| Thayer, 493 

Thaysen, 140 
Theodorescu, 313 
Thilenius, 802 
Thiroloix, 612 
Thoeni, 140 

Thom, 150 
Thompson, 241, 624, 724, 767 
Thompson, E. H., 692 
Thompson, J. C., 361 


Smith, Theobald, 21, 23, 25, 40, 53, 101 Thompson, St. Clair, 562 


Sokolowski, 234, 420, 428, 592 
Sommerfeld, 133 

Soparkar, 23 

Sorel, 756 


Thormeyer, 567 

Thue, 253, 510 : 
Tibber, 455 

_Tibbles, 743 


Sorgo, 234, 241, 253, 274, 388, 602, 770 Tobiesen, 802 


Soulignoux, 574 
Spano, 107 

Spehl, 551 

Spengler, 795, 818, 822 
Spieler, 455 
Spindler-Engelsen, 207 
Spivak, 791 

Sprawson, 769 

Squire, 475, 626, 784 
Stadler, 726 

Staehelin, 526 

Staines, 716 
Steffenhagen, 42 
Stern, F., 562 

Stern, R., 638 

Sticker, 126 

Stierlin, 565 

Stiller, 122 

Stimson, 392 
Stivelman, 824, 825 
Stockwell, 550 
Stoerck, 344 

Stokes, John H., 585 
Stokes, William, 271, 312, 794 
Stoll, 512 

Stoll, H. F., 462, 467, 469, 512 
Stone, 613 
Strandgaard, 241, 265 
Strauss, 51 

Stricker, 243, 251, 770 
Strohl, 800 
Sukienikow, 462, 463 
Sweet, 77 

Sydenham, 580 
Symmers, 588 


TacHau, 802 
Takaki, 284 
Takeya, 45 
Taute, 29 
Taylor, 638, 729 


| Todd, 257 
Tonelle, 564 
Torrey, 186 
Townsend, 580 

| Toyofuko, 146 

| Traube, 231 
Tripier, 568 
Trousseau, 569, 784 
Trudeau, 618, 696, 723 

| Tufher, 841 
Turban, 111 

| Turk, 739 

| Twitchell, 832 


U 
UHLENBROCK, 144 
Uhlenhut, 206 
Ullom, 282 
Ungermann, 57 
Urban, 642 

Vv 


VANDERVELDE, 221 
Vaquez, 569 

| Vastenburgh, 56 
Vaughan, 600 
Vehling, 153 
Verneuil, 574 
Villar, 574 
Villemin, 17, 24, 25, 284, 598 
Viole, 551 
Virchow, 770 
Vischer, 522 
Vitvitski, 522 
Vogeler, 684 





Volk, 145 
Von den Velden, 783 
Voss, 112 
WwW 
| WaGNneER, 47 


“Wallace, 785 


874 INDEX OF 

Wallgren, 586, 818 

Walsh, 361, 362, 364, 564 

Walshe, 234, 523 

Walther, 612 

Wang, 586, 666, 786 

Ware, 243 

Warnekross, 115 

Warren, 89, 136 

Warren, E., 580 

Warstat, 701 

Warthin, 108, 109 

Washburn, 22 

Watson, 629 

Webb, 114, 150, 283, 410, 682, 687, 716, 
802, 818 

Weber, 29 

Weber, E. Parkes, 638, 642, 664 

Weber, H., #50 

Weichselbaum, 51, 143, 284 

Weigert, 161, 165 

Weil, 496, 523 

Weinberg, 104, 661 

Weiss, 484 

Weisz, 629 

Weisz, M., 116 

Welch, 221 

Weller, 109 

Wells, 748, 758 

Wenckenbach, 121, 530 

West, 243, 313, 522, 524, 599 

Wetherhill, 626 

Weygandt, 578 

Wheaton, 266 

White, 95, 287, 539, 762 

Whitla, 55 

Whitney, 521 

Whitney, H. B., 78, 152 

Widal, 495, 569 

Wiedersheim, 119 

Wiese, 221 

Wilcox, 94 

Wildbolz, 393, 394 

Williams, C. Th., 148, 234, 253, 523, 618, 
758 

Williams, F. H., 359 





AUTHORS 


Williams, Mary E., 459 
Williams, R., 615 
Williams, W., 586 
Williamson, 82, 605 
Wilner, 638 

Wilson, 247 

Wincourof, 44, 451 
Winsch, 253 

Winslow, 698 
Wintrich, 404 
Wittgenstein, 116 
Wolfenden, 864 

Wolff, 253 
Wolff-Eisner, 37, 201, 322, 411, 817 
Wollstein, 51, 63, 109 
Wolman, 362, 364, 390, 391, 539 
Wood, 55 

Wood, J. W., 361 
Wood, N. K., 319 
Woodruff, 129 

Wright, A., 210, 283 
Wright, L. B., 600, 757 
Wunderlich, 603 
Wynn, 217, 459 


x 
XYLANDER, 206 

ny, 
YELD, 614 
Yeo, 150 
Ysendick, 580 

Z 


ZAHN, 522 
Zemmin, 824 
Ziegler, 361 
Ziehl, 19 
Ziemann, 73 
Zink, 833, 836 


INDEX OF SUBJECTS. 


A 


AxBortTION in phthisical women, 675 
Abortive tuberculosis, 414 
diagnosis of, 417 
physical signs of, 417 
symptomatology of, 415 
treatment of, 845 
climatic, 717 
Abscess, cold, of chest wall, 574 
ischiorectal, 182, 613 
of lung, 546 
Acid-fast bacilli, 18, 29, 30 
in blood, 284 
in milk, 57 
streptothrix, 550 
in tap water, 383 
Aecnitis, 268 
Actinomycosis of lung, 549 


Adrenals, dysfunction of, 609 
| in etiology, 114 
_Age incidence, 88, 446, 474 
| diagnosis and, 191 
morbidity and, 83 
mortality and, 85 
prognosis and, 620 
Air, stagnant, 698 
“Alarm zone,’ 379, 417 
_Albumin in sputum, 212 
_Albuminuria, 287 
Alcohol, 854 
| | Allergy, 128, 145 
Alopecia, 271 
Altitude, artificial pneumothorax and, 
810 


frequency of tuberculosis and, 76 
in pththisiotherapy, 715 
Amenorrhea, 192, 576 


Activity of disease, determination of, 190 Amyloid changes, 185 


Acute forms of tuberculosis, 424 
prognosis in, 46 '6, 620 
treatment of F 849 

miliary tuberculosis, 436 
course of, 446 
diagnosis of, 444 
meningeal form of, 441 
in adults, 442 
in children, 441 
pathogenesis of, 436 
pathology of, 438 
prognosis in, 446 


pulmonary form of, 439 


roentgenology of, 445 
traumatic, 642 
treatment of, 849 
typhoid form of, 489 
tuberculin test in, 387 
pneumonic phthisis, 430 
Addison’s disease, 610 
Adenoids and tuberculosis, 588 
Adenopathy, bovine bacilli in, 33 
cervical, 457 
tracheobronchial, 457 
in children, 457 
diagnosis of, 470 
pathology of, 168, 184 
physical signs of, 461 
prognosis in, 471 
roentgenology in, 468 
symptoms of, 457 
treatment of, 850 
tuberculin diagnosis in, 470 


of intestines, 564 
of kidneys, 287 
i Agiphorophony; 353 
Anaphylaxis, 37 
Anasarca, 288 
Anatomy, morbid, 160 
| Anemia, 281 
| Anergy, 128 
Anesthesia in artificial pneumothorax, 
833 
in phthisical patients, 652 
| Aneurysms of Rasmussen, 176, 235 
| Annular shadow, 365 
Anorexia, 258 
in advanced phthisis, 260 
causes of, 259 
| diet in, 736 
in incipient phthisis, 376 
treatment of, 790 
Antagonistic diseases, 584 
asthma, 589 
atherosclerosis, 604 
cancer, 514 
cardiac, 592 
cholelithiasis, 604 
coryza, 588 
gout, 603 
hyperthyroidism, 608 
lymphatism, 588 
nephritis, 604 
nephrolithiasis, 604 
obesity, 606 
scrofula, 584 








876 INDEX OF SUBJECTS 


Antagonistic diseases, syphilis, 598 


Anthracosis, 52 

in animals, 56 

in roentgenogram, 356 
Antiformin, 206 
Antipyretics, 778 
Apex, percussion of, 326 

Kroénig’s method, 325 

predisposition of, 117 
Apical catarrh, 538 

pleurisy, 486 
Appendicitis, 612 

and pleurisy, 485 
Appetite, 258. See Anorexia. 
Apyretic tuberculosis, 228 
Arneth’s blood picture, 283 
Arrhythmia, 280 
Arsenic, 754 
Articular tuberculosis, 586 
Ascites, 567 
Asthenic constitution, 123 
Asthma and tuberculosis, 589 
Atavistic tendencies, 123 
Atherosclerosis, 604 
Athletes, tuberculosis in, 640 
Atrepsia in infants, 451 
Auscultation, 336 


in abortive tuberculosis, 417 


in advanced phthisis, 400 
for adventitious sounds, 345 
in aged patients, 476 


in artificial pneumothorax, 814, 834 


in cancer of the lung, 548 

in children, 465 

in incipient phthisis, 379 

over cavities, 404 

in pleural effusions, 494 

in pneumothorax, 527 

single phase, 337 

sources of error in, 343 

technic of, 336 

of voice sounds, 352 

of whispered voice, 352 
Autoinoculation, 693 
Autonomic nervous system, 290 


Autopsies, reliability of statistics of, 68 
tuberculous lesions found at, 62 


Autoserotherapy, 857 
Autoserum test, 393 
Autourine test, 893 
Avian bacilli, 28 


B 


Bact, tubercle, 17 


in abortive tuberculosis, 415, 


416 
acid-fast, 18, 29 


in acute forms of tuberculosis, 


433 
atypical, 42 
avian, 28 


in human beings, 29 


avirulent, 68 


in abortive tuberculosis, 414 
in latent lesions, 86 





Bacilli, tubercle, in birds, 28, 32 


bovine, 27, 32, 58 
in children, 33, 663 
in human beings, 32, 58 
immunity to, 154 
mutation of, 41 
in phthisis, 38, 158 
prophylaxis, 663 
virulence in humans, 34, 
127 
in calcified glands, 144 
in circulating blood, 284 
in cerebrospinal fluid, 443 
channels of entry, 43 
classification of, 20 
in cold-blooded animals, 29 
cultivation of, 20 
diagnostic value of, 382 
in domestic animals, 32 
in dust, 46 
in early phthisis, 382 
in embryo, 109 
examination for, 205 
antiformin method, 208 
fatty substance in, 18 
in fibroid phthisis, 421 
in giant cells, 162 
in healed lesions, 39, 158 
in healthy persons, 51 
human, 26 
in human milk, 663 
infective dose of, 140 
in reinfection, 146 
ingestion of, 54 
inhalation of, 40 
inoculation of, 21, 44, 209 
in intestines, 54 
latency of, 148 
media for, 20 
microscopic examination for, 
in milk, 57 
morphology of, 17 
multiplication in human body, 
141 
mutation of, 41 
non-pathogenic, 29 
differentiation of, 31 
in non-tuberculous patients, 383, 
414 
number in sputum, 61, 208, 
624 
occurrence in nature, 32, 40 
in ovum, 109 
as parasites, 40 
in placenta, 106 
in pleural effusions, 509 
poisons from, 35 
powers of resistance, 21 
prognosis and, 208, 624 
pseudotubercle, 29 
grass, 30 
leprosy, 30 
smegma, 29 
trumpet, 30 


INDEX OF 


Bacilli, tubercle, in sausages, 22 
in semen, 106 
in serous membranes, 35 
sources of, 48 
spread within the body, 183 
in sputum, 205 
prognostic value of, 208, 
624 
staining of, 18, 205 
in stomach, 54 
in tonsils, 125 
toxins of, 36 
transitional, 42 
transmutation of, 42 
in traumatic tuberculosis, 642 
types of, 17, 25, 40 
ubiquity of, 61 
virulence, 24 
in abortive 
414 
in acute tuberculosis, 430 
in glands, 144 
vitality of, 23 
zoogenetic, 34 
Bacteria, pyogenic, 601 
Bacteremia, 284, 601 
after tuberculin 
770 
in miliary tuberculosis, 
non-tuberculous, 602 
in skin infections, 44 
Ballooning, 814, 815 
Basal lesions, 540 
Baths, 681 
Bell sound, 529 
Blood, 281 
bacilli in, 284 
picture, 282 
Arneth’s, 283 
in artificial pneumothorax, 812 
changes in mountains, 716 
in miliary tuberculosis, 444 
in pleural effusions, 505 
in stools, 564 
Blood-pressure, 281 
prognosis and, 624 
Bradyeardia, 280 
Breath sounds, absence of, 339 
in advanced phthisis, 401 
amphoric, 407 
in pneumothorax, 527 
bronchial, 342 
bronchovesicular, 343 
cavernous, 407 
in children, 465 
cog-wheel, 341 
feeble, 338 
granular, 340 
interrupted, 341 
metamorphosed, 408 
normal, 338 
rough, 340 
Bronchiectasis, 542 
in fibroid phthisis, 427 
in tuberculous lungs, 174 


tuberculosis, 


treatment, 391, 


437 


SUBJECTS S7i 


0 


| Bronchitis, 589 


hemorrhagic, 551 
Bronchophony, 352 
in children, 467 
in pleural effusions, 494 
Bronchopneumonia, tuberculous, 433 
complications of, 436 
diagnosis of, 436 
etiology of, 483 
hemoptysis and, 255 
in infants, 451 
physical signs of, 435 
prognosis of, 436 
symptoms of, 434 
tuberculosis and, 591 
Brownlee’s three types of phthisis, 98 
Butter in diet, 742 


CaAcHEXIA, 263 
in infants, 451 
Calcification, 165 
Calcium in diarrhea, 793 
in hemoptysis, 786 
Cancer of lung, 547 
tuberculosis and, 614 
Carbohydrates as foods, 748 


_Carcinomatosis, miliary, 446 
Cardiac diseases, 127, 552 


weakness, treatment of, 785 
Cardiovascular symptoms, 277 
‘‘Carriers,’ 208, 728 
Caseation, 164 
Caseous pneumonia, 430 
Catarrh, apical, 538 
Causes, constitutional, 101 
Cavities, pulmonary, 173 

adventitious sounds over, 408 

bacilli in, 600 

basal, 409, 540 

bleeding from, 176, 239 

breath sounds over, 407 

bronchiectatic, 174, 427, 542 

closed, 176 

cough from, 199 

diagnosis of, 403 

differentiation from pneumo- 
thorax, 531 

in fibroid phthisis, 421 

healing of, 180 

mixed infection in, 600 

pathology of, 173 

phantom, 409 

postural treatment of, 771 

prognostic significance of, 626 

roentgenology of, 365 

sputum from, 202 

treatment of, 771 

tympany over, 404 

whispered voice over, 353 


Cerebrospinal fluid, 443 


Chairs, reclining, 701 


878 


Cheese as a food, 741 
tubercle bacilli in, 21 
Chemotherapy, 747 
Chest in advanced eases, 311 
in aged patients, 476 
appearance in roentgenogram, 
357 
asthenic, 305 
asymmetry of, 308 
deformities of, 303 
enlarged veins on, 301 
flat, 303 
life insurance and, 649 
muscular changes in, 309 
normal, 301 
paralytic, 303 
phthisical, 302 
acquired, 305 
in children, 563 
congenital, 305 
pterygoid, 303 
retractions of, 308 


Children, pulmonary tuberculosis in, 447 | 


bovine infection in, 33, 663 
characteristics of, 447 


exposure to infection of, | 


192, 660 
extent of infection among, 


fat consumption in, 266 
meningitis in, 441 
prognosis in, 471 
prophylaxis in, 660 
roentgenography in, 468 
scrofula in, 454 
symptoms of, 453 
reflex, 468 

treatment of, 850 


INDEX OF SUBJECTS 


|Clubbed fingers in fibroid phthisis, 422 


354, | 


tuberculin test in, 387, 470 | 


Chloasma phthisicorum, 268 
Chlorosis, pretuberculous, 375° 
Cholelithiasis, 604 
Cholesterin in pleural effusions, 520 
Choroid, tubercles in, 445 
Cirrhosis of liver, 613 
City life and tuberculosis, 77, 97 
Civilization and tuberculosis, 61, 76 
Classification of phthisis, 368 

author’s, 371 

official, 368 

shortcomings of, 369 
Climate, infection and, 73, 76 
Climates, desert, 721 
mountain, 715 
contraindications, 718 
indications, 717 
sea, 719 

Climatic treatment, 710 

cost of, 711 

economic aspects of, 710 

effects of, 712 

vs. open-air treatment, 697 

where obtained, 714 
Clothing, 681 
Clubbed fingers, 271 





Coal miners, immunity of, 132 
Cod liver oil, 758 
administration of, 750 
contraindications, 759 
indications, 759 
Cog-wheel breath sounds, 341 
**Colds,”” 125°- 
in etiology, 125 
in history of the disease, 192 
pleurisy and, 482 
Collapse during hemorrhage, 239 
induration, 537 
in pneumothorax, 523, 816 
treatment of, 788, 817 
Coma, 442 
Complement-fixation test, 392 
prognostic value of, 629 
'Complexion, 1238, 267, 299 
| Complications of phthisis, 558 
abscess of chest wall, 574 
appendicitis, 612 
cardiac, 568 
empyema, 506 
gangrene of lung, 563 
influenza, 595 
intestinal tuberculosis, 564 
laryngeal tuberculosis, 558 
meningitis, 441 
myocarditis, 568 
nephritis, 572 
pericarditis, 568 
peritonitis, 565 
phlebitis, 569 
pleural effusions, 505 
pleurisy, dry, 500 
pneumothorax, 521 
prognosis and, 625 
purpura, 573 
pyelitis, 572 
terminal edema, 572 
thrombosis, 569 
influence on prognosis, 413 
tongue, ulcerations of, 573 
treatment of, 856 
ulcerations of mucous mem- 
branes, 573 
urogenital tract, 572 


Condiments in diet, 744 


Congenital infection, 108 
Conjugal phthisis, 149 
Constipation, 262 
treatment of, 791 
Constitutional diseases, 602 
inferiority, 122 
Contact infection, 44 
Convulsions, 443 
Corsets, 681 
Coryza, rare in tuberculosis, 588 
Cough, 195 
in abortive tuberculosis, 416 
absence of, 195 
in acute pheumonic phthisis, 431 
in advanced phthisis, 199, 398 
in aged patients, 475 


INDEX OF 


Cough in bronchial adenopathy, 457, 460 
in bronchiectasis, 199 
in children, 460 
diagnostic significance of, 200 
in early stages, 195 
emetic, 197 
treatment of, 774 
in fibroid phthisis, 425 
frequency of, 195 
hysterical, 196, 200 
in incipient phthisis, 475 
in infants, 457 
infection through, 48 
paroxysmal, 196 
prognostic significance of, 200 
psychic influences on, 200 
psychotherapy of, 772 
treatment of, 771 
medicinal, 773 
in tuberculous bronchopneumonia, 
435 
““Cough phenomenon,” 359 
Cracked-pot resonance, 406 
Creosote, 749 
administration, 751 
contraindications, 751 
derivatives from, 752 
indications, 751 
Crepitation, 346 
Cuspidors, 671 


D 


Dacry.itis, tuberculous, 455 
Death, modes of, 412 
from pulmonary hemorrhage, 
253 
in laryngeal tuberculosis, 562 
in pleurisy, 508 
premonitory signs of, 366 
rates from tuberculosis, 75, 76, 79, 
82 
Degeneration, stigmata of, 122 
Delirium, 295, 441, 443 
Demineralization, 112 
Dermographism, 267, 290 
Desert climate, 721 
D’Espine’s sign, 466 
Dextrocardia, 401 
Diabetes, 604 
artificial pneumothorax and, 833 
rarity in tuberculous, 606 
symptoms of, 605 
Diagnosis by animal inoculation, 209 
dangers of hasty, 187 
differential, 534 
from abscess of the lung, 546 
from actinomycosis, 549 
from acute endocarditis, 554 
pneumonic phthisis, 433 
from apical catarrh, 538 
from bronchiectasis, 542 
from bronchopulmonary spiro- 
chetosis, 551 





SUBJECTS 879 
Diagnosis, differential, from cancer of 
the lung, 547 
from cardiac disease, 552 
from chronic bronchitis, 541 
pneumonic processes, 539 
from collapse induration, 537 
from gangrene of the lung, 546 
from hemorrhagic bronchitis, 
551 
from hyperthyroidism, 556 
from influenza, 595 
from mitral stenosis, 552 
from neurocirculatory asthenia, 
557 
from nonspecific pulmonary in- 
fections, 539 
from pericarditis, 554 
from pleural vomice, 544 
from pulmonary infarction, 554 
streptothrichosis, 550 
from rhinopharyngeal diseases, 
535 
from syphilis of the lung, 554 
from tonsillitis, 536 
elementary principles of, 190 
history in, 191 
natural method of, 191 
Diaphragm in pneumothorax, 530 
roentgenography of, 359 
Diaphragmatic pleurisy, 483 
Diarrhea, 262, 564 
in aged patients, 476 
due to diet, 741 
emaciation and, 265 
treatment of, 792 
Diathesis, 122, 141 
arthritic, 603 
Diazo-reaction, 629 
Diet, 733 
for febrile patients, 778 
in hemoptysis, 787 
in sanatoriums, 730 
vegetarian, 738 
weight and, 734 
Dietaries, 745 
Dietetic treatment, 733 
economic aspects of, 733 
individualization in, 733 
need for special, 736 
variety in, 736 
Disability, occupation and, 637 
resulting from tuberculosis, 634 
Disease vs. infection, 61, 101, 187, 454 
Diseases, preéxisting, 192 
Domestic servants, selection of, 661 
Droplet infection, 48 
Duration of life, 411 
Dust, 131 
bacilli in, 46 
coal, 132 
effects on lungs, 46, 51, 133 
in etiology of fibroid phthisis, 420 
harmlessness of, 132 
Dusty trades, 131 
Dyspepsia, 257 


SSO INDEX OF 


Dyspepsia in advanced phthisis, 261 
frequency of, 257 

Dysphagia, 559 
in artificial pneumothorax, 820 
treatment of, 862 

Dysphonia, 559 

Dyspnea, 278 
in artificial pneumothorax, 813 
in cancer of the lung, 547 
cardiac, 593 
as a danger signal, 689 
in fibroid phthisis, 427 
high altitude and, 718 
in infants, 452 
in miliary tuberculosis, 440 
in pneumothorax, 523 
treatment of, 788 


E 
Economic conditions in etiology, 81, 89, | 


in prognosis, 630 
treatment and, 679 
Edema, angioneurotic, 267 
cachectic, 571 
in fibroid phthisis, 427 
of legs, 570 
terminal, 288, 413, 572 
Effusion. See Pleural effusion. 
iggs, diarrhea from, 262, 742 
in diet, 741 
Egotism, 295 
Elastic fibers in sputum, 210 
Ellis’s line, 492 
Emaciation, 263 
in acute phthisis, 432, 435 
in advanced phthisis, 399 
in aged patients, 475 
in arrested disease, 632 
in children, 458 
effects of, 263 
extent of, 263, 432 
in fibroid phthisis, 422 
in glandular tuberculosis, 458 
in incipient phthisis, 376 
in infants, 451 
prognostic significance of, 234 
seasonal influences, 265 


Embolism, gas, in artificial pneumo- 


thorax, 817 
pulmonary, 552 
Embryo, tubercle bacilli in, 109 
Emetin in hemoptysis, 784 
Emphysema in artificial pneumothorax, 


pathology of, 180 
pneumothorax and, 522 
pulmonary tuberculosis and, 596 
subcutaneous, 820 
subfascial, 820 

Empyema, 506 
in cancer of lung, 506, 549 
prognosis in, 519 


SUBJECTS 


/Empyema, treatment of, 857 
Endemic diseases in etiology, 127 
Endocarditis, 185 
Endocrine glands, dysfunctions of, 113, 
607 

Endotoxins, 36, 762 
Epidemiology, 61 
Epididymitis, 587 
Epithelioid cells, 162 

origin of, 163 
| Erythema induratum, 45 

nodosum, 585 
Erythrocytes, 281 
Eugenics, tuberculosis and, 111, 676 
| EKunuchism, 115, 587 
_ Euphoria, 295 

in advanced phthisis, 399 
| Kuthanasia, 295 
| Exanthemata and tuberculosis, 594 
Exercise, 692 

effects on temperature, 218 
| Exotoxins, 762 
| Expectation of life, 411 
_Expectorants, 775 
_Expectoration, 201 

in children, 201 

treatment of, 775 
_ Exposure to infection, 634, 648 

of infants, 450, 663 
life insurance and, 634, 648 

_Extrapleural pneumolysis, 841 
| _Extrapulmonary tuberculous lesions, 584 





F 


Facts, 299 
Familial tuberculosis, 450 
Family history, insurance and, 644 
| Farming, 684 
Fat consumption, 266, 607 
| in diet, 742 
intolerance of, 258 
| Fecundation, 579 
| Fertility, 298, 579 
Fetus, infection of, 108 
Fever, 213 
in abortive tuberculosis, 416 
absence of, 228 
in acute pneumonic phthisis, 432 
in advanced phthisis, 399 
after artificial pneumothorax, 811, 
823 
after hemoptysis, 255 
in aged patients, 475 
anorexia and, 218, 258 
antipyretics in, 778 
in children, 537 
chronic, in non-tuberculous diseases, 
| 223 
continuous, 225 
cyclic, 225 
diagnostic significance of, 229 
in differential diagnosis, 536 
due to complications, 229 





INDEX OF SUBJECTS 


Fever due to medication, 229 
effects of rest on, 690 
evaluation of, 221 
exercise and, 689, 692 
in fibroid phthisis, 422, 425 
in glandular tuberculosis, 458 
hectic, 226 
hydrotherapy in, 778 
hysterical, 223 
in incipient phthisis, 217, 222, 376 
influence of hemoptysis on, 254 
intermittent, 226 
irregular, 227 
medication for, 778 
menstrual, 221 
in miliary tuberculosis, 489, 444 
mixed infection in, 213 
mountain climate for, 717 
open-air treatment for, 704 
in pleurisy, 489, 501 
premenstrual, 221 
prognostic significance of, 229, 622 
provoked, 218 
psychic state and, 220 
pulse in, 278 
reaction to, 228 
rest and, 689, 692 
reverse type of, 223 
as a symptom of activity, 213 
symptoms of, 218 


in tracheobronchial adenopathy, 459 | 


treatment of, 776 
in tuberculin reaction, 390 
in tuberculous bronchopneumonia, 
434 
types of, 224 
undulating, 225 
Fibroid phthisis, 419 
course of, 423 
diagnosis of, 424 
emphysematous form, 422 
etiology, 420 
forms of, 421 
pathology of, 421 
physical signs in, 423 
pleural form, 426 
prognosis in, 428 
simple fibrosis, 424 
syphilis and, 420, 599 
treatment of, 850 
Fingers, clubbed, 271 
First born, handicap of, 110 
Fish in diet, 739, 748 
Fistula-in-ano, 613 
Fluoroscopy, 357 
of children, 469 
Folliclis, 270 
Foods, carbohydrate, 743 
condiments in, 744 
protein, 738 
Forced feeding, 734 
dangers of, 7438, 744 
precautions in, 736 
Friction sounds, 350 
J differentiation from rales, 487 


56 


(oe) 
00 
poet 


Fumes, inhalation of noxious, 136 


| Friedreich’s phenomenon, 405 


| 


G 


| GABBET’s stain, 19 
Galloping consumption, 430 
Games, indoor, 695 
| outdoor, 695 
_Gangrene of the lung, 563 
| Gastro-intestinal symptoms, 257 
in advanced phthisis, 260 
treatment of, 791 
tuberculosis and, 612 
_Genito-urinary organs, 184 
pulmonary tuberculosis and, 587 
tuberculosis of, 587 
| Genius, tuberculosis and, 297 
Geographical distribution, 76 
Gerhardt’s phenomenon, 406 
Germinative transmission, 107 
Giant cells, 160 
Glands, cervical, in apical pleurisy, 488 
enlarged, 301 
infection of, 57, 64 
mesenteric, 184 
pathology of, 168, 184 
pulmonary tuberculosis and, 586 
tracheobronchial, 168 
in roentgenogram, 356 
tuberculous. See Adenopathy. 
virulent bacilli in, 144 
Glycosuria, 606 
Gonads, 610 
| in etiology, 115 
| Gout, fibroid phthisis and, 420 
| tuberculosis and, 603 
| Graduated labor, 693 
| Graves’s disease, 608 
| Grocco’s triangle, 493 
| Growth, 575 
Guinea-pigs, spontaneous tuberculosis in, 
210 


a 





H 


Hapitvs phthisicus, 299 
in children, 463 
Hair, 271 
color of, 123 
Handkerchiefs, 673 
Hardening, 705 
of children, 851 


| Headache, 442 
| Head’s zones, 292 


| Heart, diseases of, 592 
displacement of, 401, 410, 426 
effects on tuberculosis, 593 
hypertrophy of, 592 
irritability of, 278 
palpitation of, 277 
pathology of, 185 


882 


Hectic fever, 226 
Hematemesis, 251 
Hematogenous infection, 53 
Hemophobia, 248 
Hemoptysis, 234 
in abortive tuberculosis, 416 
in abscess of lung, 546 
in acute pneumonic phthisis, 432 
respiratory diseases, 245 
in advanced phthisis, 238, 400 
in aneurysm of the aorta, 246 
in arrested disease, 631 
arthritic, 244 
in artificial pneumothorax, 812, 829 
blood-pressure and, 281 
in bronchiectasis, 246, 250, 258, 
548 
in bronchitis, 243 
bronchopneumonia after, 485 
causes of, 241 
convalescence from, 787 
deaths due to, 253 
diagnostic significance of, 243 
diet in, 787 
disability from, 636 
during lactation, 248 
menopause, 855 
tuberculin treatment, 720 
effects of, 236 
epidemics of, 242 
excitement and, 780 
exertion and, 241, 636, 780 
fatality of, 253 
in fibroid phthisis, 424, 427 
false, 244 
frequency of, 234 
from esophagus, 244, 247 
in heart disease, 245, 552 
hematemesis and, 251 
hereditary, 249 
high altitude and, 719 
hysterical, 248 
influence of, on course of disease, 
254 
in influenza, 245 
life insurance and, 647 
localization of source of, 250 
menstrual, 247, 577 
of nervous origin, 248 
in non-tuberculous diseases, 252 
at onset of phthisis, 237, 374, 377 
overexertion and, 241, 636, 780 
pathology of, 177, 235 
in pleurisy, 245, 489 
in pregnant women, 248 
premonitory symptoms of, 238 
prognostic significance of, 252, 624 
prophylaxis of, 780 
in pulmonary emphysema, 245 
infaretion, 246 
spirochetosis, 551 
in rhinopharyngeal conditions, 244 
seasonal inflences on, 242 
sexual differences and, 241 
spurious, 244 


| 








INDEX OF SUBJECTS 


Hemoptysis, stature and, 241 
streaky, 243 
symptoms of, 239 
in syphilis of lung, 246 
traumatic, 640 
treatment of, 780 
by artificial pneumothorax, 783, 
829 
posture during the, 781 
tying the extremities in, 783 
venesection in, 786 
with adrenalin, 784 
with atropin, 785 
with blood serum, 786 
with calcium salts, 786 
with camphor, 786 
with digitalis, 785 
with emetin, 784 
with ergot, 785 
with gelatin, 785 
with morphine, 782 
with nitrites, 784 
with salt, 782 
of unknown origin, 249 
Hemorrhages, intestinal, 564 
Hemorrhagic phthisis, 240 


Heredity, 103 


biological aspects of, 105 
clinical aspects of, 111 
definition of, 105 
germinative, 105 
statistics of, 103 
Hermann stain, 205 
Herpes zoster, 268 
ue shadow, 356, 358, 362 
in children, 569 
‘History of exposure, 192 
in infants, 449 
of the patient, 191 
of the present illness, 192 
prognostic significance of, 621 
| Hoarseness, 201 
in early phthisis, 377 
in laryngeal tuberculosis, 560 
in mitral stenosis, 553 
House infection, 46 
Hy dropneumothorax, 527 
roentgenography of, 366, 531 
treatment of, 859 
Hydrotherapy, 778 
| Hygiene, personal, 680 
_Hyperesthesia, 292 
in pleurisy, 483 
Hypersensitiveness to foreign proteins, 
37, 390 
phenomena of, 37 
| Hyperthyroidism, 608 
differential diagnosis of, 556 
effects on tuberculous disease, 607 
in etiology, 144 
Hypoasphyxial syndrome, 277 
| Hypotension, arterial, 281 
adrenals in, 115, 609 
in early phthisis, 377 
Hypothyroidism, 609 


le Bae 


a 


INDEX OF SUBJECTS 


IcHTHYOL, 754 
Idiocy, 294, 616 
Immunity, 138 
acquired by infection, 145 
of adults, 146, 158 
clinical evidence of, 151 
of consorts, 149, 674 
endogenous, 146 
exogenous, 145 
experimental proof of, 145 
failure of, 155 
‘father,’ 150 
of hospital staffs, 147 
“mother,” 150 
of mucous membranes, 151 
of nurses, 147 
phenomena of, 138 
phthisis a manifestation of, 153 
of physicians, 147 
of scrofulous children, 151, 454, 586 
through bovine infection, 154 
Immunization, artificial, 666 
passive, 770 
with milk, 59 
Incipient phthisis. See Phthisis. 
Incubation, period of, 451 
Indians, American, tuberculosis among, 
73 
India-rubber ball sound, 408 
Infancy, tuberculous during, 449 
diagnosis of, 452 
history of exposure in, 450 
prognosis in, 452 
prophylaxis in, 660 
symptoms of, 451 
Infantilism, 576, 611 
Infants of tuberculous mothers, 583 
extent of infection among, 


70 
newborn, freedom from 
infection of, 63, 83 


Infarction, pulmonary, 554 
Infection, tuberculous, 40 
of adults, 146 
age influence on, 62 
barriers against, 50 
‘‘benevolent,’’ 668 
channels of entry, 43, 52 
of children, 58, 62, 70, 147, 660 
congenital, 107 
of consorts, 149 
by contact, 44 
dangers of, 637 
droplet, 48 
experimental, 40 
in human beings, 152 
vs. epidemiological, 59 
vs. spontaneous, 130 
exposure to, 192, 637 
of infants, 663 
life insurance and, 648 
extent of, 70 
familial, 664 


883 


Infection, tuberculous, focal, 68 
frequency of, 62 
of glands, 33, 57 
hematogenous, 53 
of hospital staffs, 147 
housing conditions and, 47, 82 
hygienic conditions and, 92 
immunity conferred by, 59, 145 
inadequacy of, 101 
of infants, 49, 63, 70, 142, 664 
by ingestion, 54 
dose in, 141 
by inhalation, 46, 141 
by inoculation, 44, 140 
intensity of, 140 
intraovular, 106 
intrauterine, 106, 108 
latency of, 57, 63, 65, 143, 166 
lymphoid, 144 
lymphogenous, 53 
marital, 149, 674 
metastatic, 144 
mixed, 600 
of nurses, 147 
of physicians, 148 
placental, 107 
prevention of, 660 
of primitive peoples, 73 
problems of, 40 
results of, 102 
in sanatoriums, 148 
sanitary conditions and, 92 
secondary, 601 
spermatogenic, 106 
through cough, 48 
dust, 46, 51 
milk, 663 
mucous membranes, 51 
sputum, 46 
sweat, 233 
| the air, 48, 50 
| the nose, 50 
| the skin, 44 
the sputum, 46 





tonsils, 55 
vs. disease, 61, 101, 187, 454 — 
vs. spontaneous tuberculosis, 
138 


with bovine bacilli, 58, 663 
immunity through, 154 

Influenza, 539 

in etiology, 128 

prognosis and, 625 

sequels of, 542 

tuberculosis and, 595 
‘Injury. See Traumatic tuberculosis, 638 
‘Insanity and tuberculosis, 616 
Insomnia, 297 
| treatment of, 789 
‘Inspection, 299 
in children, 463 
in incipient phthisis, 377 
technic of, 305 
Institutional treatment, 723, See Sana- 
toriums, 





s 


884 INDEX OF SUBJECTS 


Intellect of consumptives, 296 
Internal secretions, 113, 607 © 
Intestines, tuberculosis of, 564 
diagnosis of, 564 
emaciation and, 265 
pathology of, 181 
symptoms of, 181 
treatment of, 792 
Ischiorectal abscess, 182, 613 


J 


Joints, bovine bacilli in, 33 
pulmonary tuberculosis and, 586 
tuberculosis of, 84, 455, 586 


K 


Kupneys, 285 
amyloid, 185 
symptoms of, 287 
tuberculosis of, 572, 587 
Kroénig’s resonant areas, 325 
in incipient phthisis, 378 


L 
Lapor, effects on the disease, 582 


Lagging, 308 
Languor, 376 


Larynx, artificial pneumothorax and, 832 | 


tuberculosis of, 558 

diagnosis of, 560 
frequency of, 558 
pathology of, 181 
prognosis in, 562 
symptoms of, 559 
treatment of, 860 

Latency of tuberculosis, 51, 57, 63, 65, 

68, 143 
Latent tuberculosis, avirulent bacilli in, 
69 

virulent bacilli in, 68 


Lesions, tuberculous, among healthy, 62 


initial, 52 
repair of, 178 
Leukocytes, 282 
Life insurance aspects, 634 
medical examination for, 643 
Lime starvation, 112 
Lips, tuberculous ulceration of, 573 
Liver, pathology of, 186 
Locus minoris resistentie, 111 
Lumbar puncture, 443 
Lung, abscess of, 546 
apex, predisposition of, 117 
bacteriology of, 50 
blocks, 83 
cancer of, 447 
cavities in, 173, 403, 627 
circulation in the, 116 
as a culture medium, 116 


| Lung, extension of lesion in, 170 

| first lesion in, 170 

gangrene of, 546 

| gross appearance of, 167 
mixed infection and, 174 
perforation of, 827 
reparative processes in, 178 
in roentgenogram, 358 
rupture of, 178, 521, 827 
size of the, 116 
tubercles in, 167 

et 584 

| Lymphatism, 588 

abortive tuberculosis and, 414 

| pulmonary phthisis and, 588 

| serofula and, 455 

_Lymphoid latency, 144 





M 


MauariA complicating phthisis, 230 
| Manometer, 800 
Manometric hints, 805 
Marital phthisis, 149, 674 
| Marriage of tuberculous, 579, 674 
| Marriages, consanguineous, 123 
Measles in etiology, 127 
tuberculosis and, 598 
Meat in diet, 738 
eating, tuberculosis and, 604 
raw, 738 
'Mediastinum, displacement of, 410, 426 
in pleural effusions, 499 
in pneumothorax, 525, 530, 814 
weak, 814 
'Medication, harmless, 747 
Medicinal treatment, 746 
importance of, 746 
'Medico-legal aspects, 634 
' Meningitis, tuberculous, 441 
| Menopause, obesity during, 266 
tuberculosis during, 855 
Menstruation, disturbances of, 577, 610 
fever and, 221 
| hemoptysis during, 247, 577 
vicarious, 248, 577 
| Mental traits, 296, 
| Mercury, 757 
Metabolism, calcium, 113 
disturbances in, 112 
Metallic tinkle, 409 
in pneumothorax, 528 
| Milk, anorexia and, 790 
as a cause of diarrhea, 262 
dangers of, 24 
| in diet, 740 
| human, tubercle bacilli in, 663 
| infections, 154 
| injections of, 57 
immunization with, 59, 154 
pasteurization of, 663 
tubercle bacilli in, 21, 30 
Miners, rarity of tuberculosis among, 133 








. Mitral stenosis, 127, 594 


INDEX OF SUBJECTS 


Mixed infection, 600 


885 


| Nocardia, 550 


in artificial pneumothorax, 822 Nose, tubercle bacilli in, 51 


excavation and, 174 
in pleurisy, 496 
Morbidity, 61, 83 
in children, 454 
vs. infection, 61, 101, 187, 454 
Morphine in hemoptysis, "782 


Nursing of infants, 661 


O 


_OsBEsiIty, 266, 606 


Mortality, age effects on, 83, 85, 448, 474 Occupation, 129 


periods of, 448 
in American cities, 76 
birth rates and, 111 
in cities, 77, 79 
in the country, 77 
decline of, 91 
causes of, 91, 96 
during childhood, 583 
in dusty trades, 132 
economic influences, 81, 89, 97, 136 
effects of special campaign on, 93 
general mortality and, 94 
housing and, 82 
influence of sex on, 78, 86, 89 
natural selection and, 96, 105 
occupation and, 89 
poverty and, 81, 97 
race influences on, 97 
sexual differences in, 86 
statistics of, 74, 90 
urbanization and, 97 
in various cities, 79 
countries, 79 
wages and, 81, 89, 98, 136 
Mountain climates, 715 
Much’s granules, 19 
staining of, 208 
Murmurs, cardiac, 593 
Muscles, hyperexcitability of, 313 
pathology of, 185 
spasm of, 309 
Myocarditis, 568 
Myoidema, 312 
Myxedema, 609 


N 
Nalits, 272 


Natural selection in tuberculosis, 96, 105 | 


Negroes, African, 74 

American, 24 
Nephritis, 287, 604 
Nephrolithiasis, 604 
Nervous symptoms, 289 

system, autonomic, 290 

effects of tuberculosis on, 185 

Neurasthenia, 289 
Neurocirculatory asthenia, 556 
Nightsweats, 231 

in aged patients, 476 

causes of, 231 

in children, 459 

in incipient tuberculosis, 377 

symptomatology of, 232 

treatment of, 779 


diagnosis and, 191 
disability and, 637 
dusty, 131 
indoor vs. outdoor, 685 
suitable for tuberculous, 683 
Ochrodermia, 282 
Onset of phthisis, 192, 374 
acute, 431 
prognosis and, 622 
with hemoptysis, 237 
with pleurisy, 374, 482 
Open air schools, 852 
treatment, 696 
of children, 851 
contraindications, 707 
of febrile patients, 704 
results obtained from, 706 
technic of, 699 
vs. climatic, 697 
where obtainable, 696 
Operations, surgical, 625, 642, 833 
Ophthalmoreaction, 389 
Opiates for cough, 774 
_Opsonic index, 283, 395 
Optimism, 296 
Osseous tuberculosis, 586 
Osteoarthropathy, pulmonary, 274 
Overfeeding, 734 
precautions necessary while, 737 
symptoms of, 737 
Ovum, tubercle bacilli in, 109 
Ozone, 715 


P 


| Parns, 291 
in artificial pneumothorax, 818 
in chest, 291 
treatment of, 789 
in pleurisy, 483 


| Palpation, 299 


“light touch,’’ 307 
technic of, 305 
for vocal fremitus, 312 


_Palpitation, cardiac, 277 


causes of, 278 

| Parrot’s law, 168 
Pasteurization of milk, 663 
Pathology, 160 
'Pectoriloquy, 409 
Percussion, 314 

in abortive tuberculosis, 417 

in advanced phthisis, 400 

in aged patients, 476 

aims of, 314 


S86 INDEX OF SUBJECTS 


Percussion, apical, 325 
auscultation and, 314 
in bronchial adenopathy, 465 
in children, 465 
comparative, 320 
diagnostic value of, 335 
hooked-finger, 320 
in incipient phthisis, 323, 378 
over a cavity, 404 
in pleural effusions, 490 
pleximeter finger in, 318 
in pneumothorax, 527 
respiratory, 324 
sources of error in, 329, 334 
technic of, 316 
tidal, 332, 490 
in pleurisy, 491 
topographical, 325 
Percutaneous tuberculin test, 388 
Pericarditis, 568 
Perichondritis, 559 
Peritoneum, pathology of, 182 
Peritonitis, tuberculous, 565 
acute, 566 
adhesive, 567 
chronic, 566 
pathology of, 182 
symptoms of, 566 
Personal hygiene, 680 
Phlebitis, 569 
Phototherapy, 708 
Phrenikotomie, 843 
Phthisiogenesis, 101, 138 
Phthisiophobia, 669 


Phthisis acquired during childhood, 142. 


acute forms of, 429 
pneumonic, 430 
course of, 432 
diagnosis of, 433 
physical signs of, 432 
symptoms of, 431 
advanced, 396 
afebrile, 399 
auscultation in, 400 
duration of, 410 
euphoria in, 399 
oscillating course of, 397 
physical signs of, 400 
symptoms of, 398 
treatment of, 845 
in aged, 474 
course of, 477 
diagnosis of, 477 
etiology of, 474 
frequency of, 474 
physical signs of, 476 
symptoms of, 476 
treatment of, 854 
classification of, 272, 368 
clinical forms of, 367 
curability of, 618 
a distinctly human disease, 139 
factors predisposing to, 101 
fibroid, 419. See Fibroid phthisis. 
hemorrhagic, 240 





| Phthisis, hyperthyroidism and, 556 


incipient, 374 
course of, 396 
curability of, 618 
diagnosis of, 381 
complement-fixation test 
in, 392 
elements of, 381 
roentgenography in, 393 
sources of error in, 381 
treatment of, 844 
tuberculin test in, 384 
latency of, 143 
a manifestation of immunity, 153 
marital, 149, 674 
natural resistance against, 414 


- onset of, 474 


oscillating course of, 397 
pathology of, 167 
physical signs of, 377 
polymorphism of, 367 
rarity in children of, 477, 665 
remissions in, 397 
scrofula and, 455 

stages of, 368 

stigmata of, 299 
traumatic, 639 
treatment of, 844 


| Pityriasis tabescentium, 269 


| 
| 


versicolor, 269 


| Placenta, tubercle bacilli in, 108 
Placental transmission, 108 


| Ple 





ura, accommodative powers of, 525 


anatomy of, 478 

infection of, 578 

pathology of, 181, 479 

In roentgenogram, 366 

rupture of cavity into, 178, 523 
tuberculosis of, 478, 481 


Pleural adhesions, 502 


artificial pneumothorax and, 
834 
diagnosis of, 502, 834 
pathology of, 480 
roentgenography of, 583, 834 
thoracoplasty in, 842 
thoracoscopy for, 835 
effusions, 489 
in acute phthisis, 498 
in artificial pneumothorax, 821 
in cancer of the lung, 548 
in chronic phthisis, 501, 505 
symptoms of, 501 
during the course of phthisis, 
505 

exploratory puncture in, 495 
hemorrhagic, 505 
interlobar, 497 
physical signs of, 490 
in pneumothorax, 527 
primary, 489 
purulent, 506 

prognosis in, 508 519 

symptoms of, 506, 
in roentgenogram, 366 


INDEX OF SUBJECTS 


Pleural effusions, tubercle bacilli in, 510 
shock, 816 
vomice, 544 
Pleurisy, 481 
in acute phthisis, 499 
apical, 486, 488 
appendicitis and, 612 
in artificial pneumothorax, 821 
beneficial, 515 
in chronic phthisis, 500 
diaphragmatic, 483 
dry, 481 
exudate in, 495 
cytology of, 496 
fatal, 508 
hemoptysis in, 245 
idiopathic, 482 
initial, 482 
interlobar, 485 
life insurance and, 646 
non-specific, 514 
at onset of phthisis, 374 
pains in, 483 
primary, 481, 508 
prognosis in, 507, 515, 518 
recurrent, 486, 488 
roentgenography of, 496 
statistics of, 512 
sudden death in, 509 
traumatic, 639 
treatment of, 856 
varieties of, 481 
with effusion, 489 
course of, 498 
physical signs of, 490 
Pleximeter, 318 
hooked finger, 320 
Pneumokoniosis and lung apex, 117 
roentgen findings in, 446 
tuberculosis and, 131 
Pneumonia, apical, 433 
broncho-, tuberculosis and, 591 
caseous, diagnosis of, 433 
pathology of, 169 
prognosis in, 620 
symptoms of, 481 
lobar and tuberculosis, 591 
Pneumoperitoneum, 821 
Pneumothorax, 521 
artificial, 794 
absorption of gas in, 809 
in advanced phthisis, 829 
age of the patient and, 833 
altitude and, 810 
apparatus for induction of, 798 
bilateral, 836 
blood picture in, 812 
Brauer’s method, 797 
cardiac disease and, 833 
cases suitable for, 835 
complications of, 815, 838 
active lesion in untreated 
side, 828 
during operation, 816 
emphysema, 819 





887 


Pneumothorax, artificial, complications 
of, emphysema, 
deep, 820 
interstitial, 821 
mediastinal, 820 
subcutaneous, 819 
subfascial, 820 
empyema, 823 
gas embolism, 817 
hemoptysis, 830 
pains, 818 
perforation of the lung, 827 
pleural effusion, 821 
bilateral, 824 
septic, 823 
symptoms of, 822 
treatment of, 826 
shock, 818 
spontaneous pneumothorax, 
818 
contraindications, 832 
diabetes and, 833 
diagnostic, 831 
duration of treatment, 836 
dyspnea in, 813 
fever in, 823 
Forlanini method, 797 
frequency of refills, 810 
gas embolism in, 817 
used for inflation, 802 
for hemoptysis, 783 
hemostatic effects of, 812 
history of, 794 
in incipient cases, 832, 839 
indications for, 828 
induction of, 797 
injection in, selection of point 
for, 803 
intrapleural pressure in, 800 
in laryngeal tuberculosis, 832 
limitations of, 837 
local anesthesia in, 804 
manometer in, 800, 805 
manometric hints in, 805 
Murphy’s method, 797, 808 
needle for, 802 
open incision method, 797 
partial, 836 
perforation of lung in, 827 
physical signs of, 813 
pleural adhesions and, 834 
shock in, 818 
pheumoperitoneum in, 821 
pregnancy and, 833 
principles underlying 
ment, 795 
proportion of cases suitable for, 
835 


treat- 


pupils in, 291 

pyothorax in, 823 
treatment of, 826 

roentgenography in, 815 

selection of cases for, 828 

surgical operations and, 833 

symptoms of, 810 


888 


Pneumothorax, artificial, technic of, 797 
of insufflation, 805 
\ of refilling, 808, 810 
in urgent cases, 808 
thoracocentesis in, 804 
ultimate results in, 839 
spontaneous, 521 
in artificial pneumothorax, 818 
diagnosis of, 528 


displacement of organs in, 524 | 


double, 526 
effusion in, 527 
frequency of, in phthisis, 523 
latent, 526 
localized, 531 
mechanism of, 524 
mute, 526 
partial, 526 
pathology of, 524 
physical signs of, 526 
prognosis in, 533 
‘“providential,”’ 523 
recurrent, 522 
roentgenography in, 530, 532 
symptoms of, 523 
traumatic, 639 
treatment of, 858 
valvular, 524 
Poisons of tubercle bacilli, 35 
Polyserositis, 509 
Polyuria, 286 
Post-tussive suction sound, 408 
Poverty, prognosis of phthisis and, 81, 
630 


Predisposition, 101 
anatomical factors and, 115 
constitutional factors and, 101 
environmental factors, 101 
hereditary, 103 
of the lung, 115 
apex, 117 
nature of, 155 
occupational, 129 
stigmata of, 122 
Pregnancy, 579, 675 
artificial pneumothorax and, 833 
prevention of, 675 
Preéxisting diseases, 124 
acute infectious, 127, 594 
asthma, 126 
bronchial, 126 
cardiac, 137 
influenza, 128, 595, 625 
measles, 127, 595 
pleurisy, 125, 481 
pulmonary, 126 
syphilis, 599 
typhoid fever, 129, 598 
whooping cough, 127 
Prognosis, 618 
in abortive tuberculosis, 414, 619 
activity of the disease in, 622 
in acute forms of tuberculosis, 620 
age in, 620 
in arrested disease, 631 


INDEX OF SUBJECTS 


' Prognosis, bacilli in sputum and, 624 
cavities and, 626 
in children, 471 
complement-fixation test in, 629 
complications and, 624 
diarrhea and, 625 
economic conditions and, 630 
elements of, 619 
emaciation and, 264, 632 
extrapulmonary tuberculous lesions 

and, 584 

fever and, 229, 622 
glandular tuberculosis and, 586 
hemoptysis and, 252, 624 
heredity and, 621 
history of patient and, 621 
importance of, 618 
in infants, 452 


| "intestinal tuberculosis and, 625 


labor and, 582 
in laryngeal tuberculosis, 56 
onset of the disease and, 622 
physical signs in, 626 
pleurisy and, 625 
pregnancy and, 579 
puerperium and, 582 
pulse rate and, 623 
sex and, 621 
side affected and, 627 
special tests in, 629 
surgical operations and, 625 
symptomatology and, 622 
tuberculous kidneys and, 587 
skin lesions and, 584 
in various forms of phthisis, 619 
Prophylaxis, 660 
in adults, 667 
by artificial immunization, 666 
in children, 664 
of disease, 668 
duties of the community in, 673 
failure of, 95 
in infants, 661 
of infection, 660 
marriage and, 674 
of reinfection, 665 
| Protein foods, 738 
_Pseudotubercle bacilli, 29 
Psychasthenia, 289 
Psychic traits, 294 
Psychotherapy, 656, 658 
of cough, 772 
with medication, 747 
with tuberculin, 768 
Puberty, 576 
in etiology, 115 
tuberculosis and, 611 
Pulmonary osteoarthropathy, 274 
Pulse rate, 278 | 
instability of, 278 
prognosis and, 623 _ 
Puncture, exploratory, 495 
Pupil in acute miliary tuberculosis, 443 
in apical pleurisy, 481, 486 
in artificial pneumothorax, 291 


INDEX OF SUBJECTS 


Pupil, dilatation of, 290 
Purpura, 573 

Pyelitis, 572 
Pyopneumothorax, 506, 823 


Q 
Quartz lamp in therapy, 708 


R 


Racrau mixture and tuberculosis, 123 
susceptibility, 73 
Rales in abortive tuberculosis, 417 
in advanced phthisis, 402 
after hemoptysis, 402 
atelectatic, 351 
consonating, 348 
crepitant, 346 
in incipient phthisis, 380 
latent, 349 
moist, 347 
localization of, 348 
over cavities, 408 
pleural effusions, 494 
in pneumothorax, 831 
provoked, 349 
sibilant, 349 
sonorous, 349 
spurious, 351 
Reinfection, 145 
autogenous, 156 
endogenous, 146, 156 
exogenous, 145, 156 
in hospital inmates, 147 
metastatic, 156 
modes of, 147 
prevention of, 665 
Renal function, 286 
Rest cure, 687 
contraindications for, 691 
exercise and, 688 
indications for, 688 
principles of, 687 
technic of, 691 
Rheumatism and tuberculosis, 602 
Roentgenography, 354, 361 
in acute miliary tuberculosis, 445 
in advanced phthisis, 365 
of apex, 359, 361 
in artificial pneumothorax, 815 
cavities in, 365 
in children, 468 
diaphragm in, 359 
of hilus shadow, 356, 358, 362 
in incipient phthisis, 383 
in interlobar effusions, 504 
limitations of, 364 
lungs in, 358 
normal chest in, 354, 357 
of pleura, 496 
of pleural adhesions, 503 
in pleurisy, 496 


889 


Roentgenography in pneumothorax, 530, 
532 


sources of error in, 363 
in tracheobronchial adenopathy, 465 
Roentgen rays in therapy, 709 


Ss 


‘Sat in diet, 743 
Scarlet fever, 594 
Sclerosis, 166 
Scrofula, 454, 586 
prognosis in, 456 
relation to pulmonary tuberculosis 
456, 586 
Sanatoriums, 723 
abortive tuberculosis in, 415 
causes of failure of, 729 
cost of, 727 
diet in, 730, 733 
educational value of, 728 
inadequacy of, 725 
indications for, 731 
infection in, 148 
lasting results in, 726 
life insurance and, 647 
non-tuberculous cases in, 415, 584 
prophylactic value of, 728 
scope of, 723 
Sea climates, 719 
voyages, 720 
Sex glands in etiology, 115 
hemoptysis and, 241 
mortality according to, 86 
in prognosis, 621 
Sexual characters, secondary, 577 
excesses, 578 
functions, 578 
sphere, 298 
‘Semen, tubercle bacilli in, 107 
Shoulder, pain in, 488 
Silicosis, 135 
Skin, 266 
bronzing of, 114, 268 
eruptions, 270 
immunity of, 45 
infection through, 44 
inspection of, 301 
lesions, tuberculous, 534 
Smallpox, 595 
‘Smegma bacilli, 29 
Smith’s sign, 467 
‘Smoking, 682 
Softening of lesion, 165 
Specific treatment, 761 
| Spermatogenic infection, 106 
| Spes phthisica, 296 
Spina ventosa, 455 
Spinal muscles, sign of, 490 
| Spirochetosis, bronchopulmonary, 551 
| in gangrene of the lung, 563 
Spleen, 185 
| Sputurn, 202 
| in abortive tuberculosis, 416 


890 INDEX OF 


Sputum in abscess of the lung, 546 
in advanced phthisis, 202 
albumin in, 212 
animal moculation of, 209 
bacilli in, 204 
chemical examination of, 212 
collection of specimen, 204 
cytology of, 212 
disposal of, 671 
elastic fibers in, 210 
examination of, 204 
fetid, 546, 563 
in fibroid phthisis, 423 
flasks, 672 
in gangrene of the lung, 546, 563 
inhalation of, 46 
microscopic examination of, 204 
spirochetes in, 551 
streaky, 243 

in arrested disease, 632 

Stature, 575 
hemoptysis and, 241 

Status bacillaris, 109 
thymico-lymphaticus, 588 

Stigmata of phthisis, 299 

Stomach, dilatation of, 260 
tubercle bacilli in, 54 

Stomatitis, aphthous, 413 

Stone in gall-bladder, 604 
in kidney, 604 

Street-sweepers, rarity of tuberculosis 

among, 133 

Streptothrichosis, pulmonary, 550 

Succussion sound, 528 

Suggestion, amenability to, 295 
in treatment, 657 
with tuberculin administration, 657, 

769 

Sunlight, artificial, 708 

Superalimentation, 734 
dangers of, 748, 744 
precautions in, 737 

Surgical operations, traumatic tubercu- 

losis and, 642 
in tuberculous, 625 
in artificial pneumothorax 
and, 833 

Sweats, 231 

Symptomatic treatment, 771 

Symptomatology, 187 
importance of, 194, 370 

Symptoms, constitutional, 190, 370, 536 

Syphilis and fibroid phthisis, 420 
of the lung, 554 
and tuberculosis, 598 


T 


TACHYCARDIA, 278 
in abortive tuberculosis, 416 
causes of, 280 
high altitude and, 718 
in incipient phthisis, 377 
paroxysmal, 279 


SUBJECTS 


Tachycardia, permanent, 279 
prognosis and, 623 . 
treatment of, 788 
Tattooing, infection through, 44 
Temperature, 213. See Fever. 
frequency of taking, 215 
instability of, 220 
normal, 216 
oral vs. rectal, 214 
subnormal, 227, 231 
technic of taking, 214 
types of, in phthisis, 224 
Tents, 699 
Thermometers, 213 
Thoracoplasty, 841, 842 
Thoracoscopy, 835 
Thorax. See Chest. 
asymmetry of, 308 
deformities of, 303 
normal, 301 
phthisical, 302 
stenosis of upper aperture of, 118 
Thrombosis, 569 
of femoral vein, 570 
diagnosis of, 571 
of jugular vein, 571 
prognosis in, 571 
Thyroid, dysfunctions of, 607 
in etiology, 114 
| Timothy-grass bacilli, 30 
| Tobacco, use of, 682 
Tongue, tuberculous ulcers of, 573 
Tonsillitis and tuberculosis, 587 
Tonsils, infection through, 55 
Toxins, hypersensitiveness to, 37, 390, 763 
tuberculous, 36 
Trachea, displacement of, 410 
| Tracheobronchial adenopathy, 454 
| cough in, 460 
diagnosis of, 461 
emaciation in, 458 
fever in, 458 
prognosis in, 471 
roentgenography in, 468 
treatment of, 851 
tuberculin diagnosis in, 470 
Tracheophony, 466 
Traumatic tuberculosis, 638 
after surgical operations, 642 
clinical aspects of, 640 
expert testimony in, 6438 
pulmonary, 639 
tubercle bacilli in, 641 
Treatment of abortive tuberculosis, 844 
of acute forms of tuberculosis, 849 
of advanced phthisis, 845 
of arrested cases, 848 
climatic, 710 
cost of, 711 
economic aspects of, 710 
effects of, 712 
of febrile patients, 777 
vs. open air treatment, 697 
of complications, 856 
of convalescents, 848 





INDEX OF 


Treatment of dietetic, 733 
of children, 852 
of fibroid phthisis, 850 
of incipient phthisis, 844 
indications for, 652 
individualization in, 729 
institutional, 723 
medicinal, 746 
in advanced phthisis, 846 
of cough, 773 
of hemoptysis, 783 
open-air, 696 
abuses of, 705 
contraindications, 707 
operative, 794 
pneumothorax, 794 
psychic influences in, 656 
specific, 761 
suggestion in, 656 
symptomatic, 771 
tuberculin, 761 
of tuberculosis in aged, 854 
in children, 850 
during the menopause, 855 
Tubercle, anatomical, 160 
calcification of, 165 
caseation of, 164 
fate of, 166 
healing of, 178 
histogenesis of, 164 
necrosis of, 165 
sclerosis of, 166 
softening of, 165 
structure of, 160 
Tuberculides, 45, 270 
Tuberculin, 36 
action of, 36, 763 
antibodies in, 37 
chemistry of, 36 
clinical effects of, 390, 766 
dangers of, 770 
diagnostic value of, 391 
dilutions of, 766 
dosage of, 391, 762, 766 
hypersensitiveness to, 37, 389 
preparation of, 36, 766 
reaction of, 37, 385, 769 
bacteremia after, 391, 770 
cutaneous, 386 
focal, 385, 390 
general, 385, 390 
local, 385 
as a specific remedy, 761 
specificity of, 38, 387, 761 
tests, 37 
in adults, 72 
in children, 72, 387, 470 
clinical value of, 391 
conjunctival, 389 
diagnostic value of, 391 
in infants, 452 
specificity of, 387, 390 
subcutaneous, 389 
treatment, 761 
administration, 766 





SUBJECTS 891 


Tuberculin treatment in children, 854 
dangers from, 769 
dilution in, 766 
dosage, 766 
evidence of inefficiency, 766 
hemoptysis during, 720 
inefficacy in animals, 764 
lack of statistics of, 766 
psychic effects of, 657, 768 
reaction during, 769 
tolerance of, 763 

Tuberculolysins, 37 

Tuberculosis verrucosa cutis, 585 

Tuberculotoxins, 35 

Typhoid fever in etiology, 128 
tuberculosis and, 598 


U 


Utcers, tuberculous, of intestines, 181, 
262 
of mucous membranes, 573 
of stomach, 261 
Urban life, tuberculosis and, 77, 97 
Uremia, 288, 572 
Urinary system, 285 
Urine, tubercle bacilli in, 285 
antigens in, 393 
Urochromogen reaction, 629 
Urogenital tract, tuberculosis in, 572 


Vv 


VACCINATION and tuberculosis, 595 
Vas deferens, tuberculosis in, 587 
Veins, enlarged, on chest, 301 
in children, 464 
thrombosis of, 569 
Vagotonia, 259 
Venesection in hemoptysis, 786 
in pneumothorax, 859 
Ventilation, 698 
Virgin soil, 152 
Vocal fremitus, 312 
in pleural effusions, 494 
Voice sounds, 352 
Vomiting, 198 
after cough, 197 


Ww 


Waaegs, tuberculosis and, 82, 89, 98, 136 
War, effects of, 82, 89 

primitive races in, 74 
Weight of children, 458 

of patients, 265 

seasonal influences on, 265 
Whispered voice, 352 

in early phthisis, 381 

Williams’s tracheal tone, 405 
Wintrich’s phenomenon, 359 


Z 
ZOMOTHERAPY, 738 


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